Fecal Incontinence Diagnosis and Treatment - part 3 docx

demonstrates that in women with ultrasonographic
confirmation of sphincter defects, approximately
90% involve the external anal sphincter [101,
124–128], either in isolation or combined with rup-
ture of the internal anal sphincter. Isolated internal
anal sphincter defects are much less common,
accounting for 10% or less of all defects in the major-
ity of studies [101, 124–128]. In the absence of an
overt tear (i.e. an intact perineum), it is presumed
that such isolated defects in the internal anal sphinc-
ter result from shearing forces imposed during deliv-
ery [97].
Aside from sphincter damage, the branches of
the pudendal nerve, which contains both motor and
sensory fibres, are vulnerable to stretch or com-
pression injury, which may occur during childbirth
[157–163] when pelvic floor descent and progres-
sion of the foetal head towards the pelvic outlet may
stretch the nerve as it emerges from Alcock’s canal,
where its course is relatively fixed along the pelvic
sidewall [95]. Multiparity, instrumental delivery
(notably forceps), protracted second stage of
labour, anal sphincter tears and high birthweight
are identified risk factors [97, 123, 148, 157, 160]. In
respect to parity, first vaginal delivery appears,
from the results of prospective studies, to be the
most injurious to sphincter [5, 120, 123, 135] and
neural [123, 160] integrity alike, with damage to the
pudendal nerves being cumulative with successive
deliveries [110, 123, 153, 158, 159, 163]. Important-
ly, studies assessing pudendal nerve function in

patients undergoing emergency versus elective Cae-
sarean have shown that a section performed after
the onset of labour (especially during the later
stages) does not protect against neural damage [97,
156, 164], especially on the left side [97, 156, 160],
although the significance of this is unclear. Associ-
ation between pudendal neuropathy and symptoms
of incontinence acquired following childbirth has
been shown in some [98, 154, 159, 161, 165] but not
all [97] studies. Prolonged nerve terminal motor
latencies are a surrogate marker of pudendal neu-
ropathy and are used as a measure of demyelination
(and also axonal injury), and have been demon-
strated in 16–
30% of primiparous women at around
6 weeks following childbirth [97, 98, 123, 156, 165].
Although latencies may recover with time [97, 152,
157, 160] (i.e. suggesting that the nerve may recover
from initial injury), it is feasible that with multipar-
ity [110, 123, 153, 158, 159, 163]–perhaps chronic
straining at stool [163, 166, 167] and, indeed, ageing
[45]–neuropathy may be cumulative and thence
become an independent risk factor resulting in
symptoms [153]. It may certainly constitute one of
the multiple aetiologies contributing to inconti-
nence in parous women presenting in later life [92,
94, 129–131].
Anal Surgery
After obstetric trauma, the most common aetiologi-
cal factor associated with the development of

acquired faecal incontinence is anal surgery [145].
This is particularly the case in men; a recent retro-
spective review of 154 incontinent male patients
revealed that previous anal surgery was reported by
50% [92]. Of the 76 men in this cohort in whom only
a single risk factor was evident in their histories, anal
surgery was reported by 59%. In such procedures, it
is primarily the internal (rather than external) anal
sphincter that is susceptible to disruption, either
deliberately (e.g. lateral sphincterotomy) or as a
complication (e.g. haemorrhoidectomy) [92, 168]. In
54
S.M. Scott, P.J. Lunniss
Table 6. Type of anal sphincter disruption identified on endoanal ultrasound
Author Date Number Isolated Isolated Combined All EAS
of defects IAS EAS IAS/EAS defects %
defects % defects % defects %
Sultan et al. [97] 1993 28 46 18 36 56
Abramowitz et al. [101] 2000 39 10 85 590
Faltin et al. [124] 2000 42 5 71 24 95
Chaliha et al. 105] 2001 59 17 59 24 83
Belmonte-Montes et al. [125] 2001 28 0 66 34 100
Nazir et al. [126] 2002 14 7 79 14 93
Pinta et al. [127] 2004 17 12 65 23 88
Damon et al. [128] 2005 66 0 74 26 100
Summary data: median (range) 33.58.568.524 91.5
(14–66)(0–46)(18–85)(5–36)(56–100)
IAS internal anal sphincter, EAS external anal sphincter
Chapter 4 Risk Factors in Faecal Incontinence
both genders, the relative incidence of anal surgical

procedures has been reported to be almost identical
[92], with haemorrhoidectomy the most frequent
procedure reported, followed by fistula surgery and
sphincterotomy for anal fissure.
Lateral Internal Anal Sphincterotomy
Internal sphincterotomy was introduced into surgi-
cal practice more than 50 years ago [169], with the
lateral subcutaneous sphincterotomy becoming the
procedure of choice after it was first reported by
Notaras in 1969 [170]. This represents a “controlled”
division of the internal anal sphincter in its caudal
part, usually to the dentate line. Although lateral
internal sphincterotomy remains the surgical treat-
ment of choice for chronic anal fissures unresponsive
to medical therapy, with healing rates of up to 97%
reported [171–174], it carries a well-recognised and
significant risk of disturbance of anal continence.
Several large studies (>200 patients) have shown
that between 23% and 45% of patients will suffer
some degree of incontinence in the postoperative
period [171, 175, 176]. In the largest of these studies,
by Khubchandani et al. [171], the reported incidence
of flatus incontinence, soiling and solid stool incon-
tinence in 829 patients responding to a postoperative
questionnaire was 35%, 22% and 5%, respectively.
Others, however, reported a much lower incidence of
incontinence (only 1.4% with loss of control of flatus)
following “tailored” surgery, aimed to preserve more
sphincter by selecting the height of sphincter to be
divided [177]. Long-term studies show that problems

with continence may be transient in the majority; for
example, Mentefl et al. [174] reported a reduction in
incontinence from 7.4% in the immediate postopera-
tive period to 2.9% at 12 months. However, several
reports show an incidence of 8–18% of “any” anal
incontinence at follow-up ranging from 4.3–5.6 years
[172, 178, 179]. Although for solid stool incontinence
the incidence may be low in the long term (0–3%
[175–177,
180]), flatus incontinence may remain a
common problem, with published rates of up to 30%
[180].
With regard to pathophysiology, in the majority of
cases, this is due to extended division of the internal
anal sphincter beyond the therapeutic intention of
the surgery [175, 181]. This is consistent with the pre-
dominance of passive faecal incontinence observed
in the majority [92]. Using ultrasound, Lindsey et al.
[181] demonstrated overextension of the sphinctero-
tomy in 15/17 patients with incontinence; in four
patients, division of the internal anal sphincter was
evident throughout the length of the anal canal. Sul-
tan et al. [182] similarly showed complete division of
the internal anal sphincter in nine of ten women
though in none of the four men; they suggested this
was related to a shorter anal canal length in women.
Iatrogenic external anal sphincter injury has also
been reported in patients having undergone internal
sphincterotomy [181, 183]. Furthermore, a high inci-
dence of coexisting (occult) sphincter defects are

present in patients who develop incontinence after
sphincterotomy, even in those in whom the proce-
dure has been performed satisfactorily [184]. Indeed,
Casillas et al. [181] have reported a higher risk of
incontinence following sphincterotomy in women
who have had two or more vaginal deliveries, sup-
porting the concept that occult injury contributes to
the pathophysiology of disturbed continence in this
group [180]. Manometrically, there may be a reversal
of the pressure gradient within the anal canal; Zbar et
al. [185] suggested that pathophysiology is more
complex still, with disturbances to the rectoanal
inhibitory reflex, a shorter high-pressure zone and
more anal sphincter asymmetry.
Anal Dilatation
Although first described almost two centuries ago,
anal dilatation became the primary treatment for
anal hypertonia associated with chronic fissure-in-
ano and haemorrhoids after the introduction of the
now-infamous Lord’s procedure [originally an eight-
finger (!) anal stretch] in 1968 [186]. The concept was
that forceful dilatation would loosen the sphincter
muscle and increase blood flow to the anoderm
[187]. Despite reported success rates with respect to
pain relief of 55–80% [188–190], it is now well docu-
mented that this procedure is frequently associated
with compromised continence. Furthermore, symp-
tom recurrence may be high over the long term [189,
191].
In prospective studies, minor incontinence (soil-

ing and flatus) rates of 13–27% have been reported
immediately following dilatation [189, 192–194].
However, a study by Konsten and Baeten with medi-
an follow-up of 17 years in 39 patients who had
undergone dilatation and haemorrhoidectomy and
44 patients who had undergone dilatation alone
showed a long-term incontinence rate of 52% [191].
Comparative studies have shown that anal dilatation
is associated with a greater incidence of postinter-
vention incontinence than is sphincterotomy [192,
195, 196].
Compatible with primarily passive incontinence
noted after dilatation, impairment of internal anal
sphincter function has been shown manometrically
[197], and in symptomatic patients, internal anal
sphincter disruption, or indeed fragmentation,
55
appears to be an almost invariable finding. Speakman
et al. [198], using ultrasonography, showed that 11 of
12 patients with incontinence following anal stretch
had internal anal sphincter defects and the internal
anal sphincter was extensively fragmented in ten of
these 11. Similarly, Lindsey et al. [181] demonstrated
that in 27 patients with incontinence after dilatation,
100% had internal anal sphincter injury; the smooth
muscle ring was thinned posteriorly in ten, disrupted
posteriorly in 12 and fragmented in five. Of note, they
also reported external anal sphincter injury in eight
the 27 patients. Occult injury may also be significant,
with the potential to impact later in life. Nielsen et al.

[193] showed that 11 of 18 continent patients had
sphincteric damage (nine internal anal sphincter, one
external anal sphincter and one combined sphincters)
following dilatation and concluded that sphincter
injury may occur in more that 50% of patients under-
going this procedure, although relatively few develop
symptoms immediately.
As long ago as 1992, the use of anal dilatation was
questioned because of the risk of developing inconti-
nence [189], and there is now consensus opinion that
this is an outmoded procedure that should be aban-
doned [145, 187, 191, 196].
Fistula Surgery
Treatment for fistula-in-ano is diverse, with no single
technique being universally effective. The major
approach is surgical, with the aim of abolishing the
primary track and draining any secondary tracks.
Although sphincter-preserving techniques are
preferable, surgical division of sphincteric muscula-
ture is unavoidable in many cases, and this carries
with it the risk of iatrogenic incontinence; indeed, the
development of incontinence may be almost
inescapable after complex anal fistula surgery [145].
Fistulotomy is the classic operation for anal fistulas,
in which the track is laid open; however, this involves
division of those muscle fibres enclosed by the track.
Alternatively, fistulectomy involves excision of the
track. Seton threads may also be used, often as part of
a staged fistulotomy procedure, either as a long-term
loose draining seton or as a tight or “snug” cutting

seton [199], which provides slower division of the
enclosed muscle.
Overall, irrespective of surgical technique, retro-
spective studies in large patient series’ (200–700),
often with long-term follow-up, have shown postop-
erative incontinence rates ranging from, at best,
4–7% [200, 201] to 26–45% [202–204]. More specifi-
cally, impairment of continence following fistuloto-
my has been reported in up to 54% of patients,
whether by lay-open technique [202, 205, 206] or
through a cutting seton (see review by Hammond et
al. [199]) [205, 207–209]. Certainly, the higher the fis-
tula, the greater the potential for impaired function
after fistulotomy. However, even in patients where
the consequences of sphincter division would be
anticipated to result in minimal functional distur-
bance (i.e. with low fistulas), incontinence may still
occur due to the additive effects of other risk factors,
such as previous obstetric injury in women [181].
Importantly, postoperative incontinence is more
common than fistula recurrence, and rates of dissat-
isfaction with surgery may thus be attributable to
such disturbances in continence [204].
Mechanistically, various studies have shown that
patients who are incontinent following fistula sur-
gery have reduced resting tone in the distal 1 or 2
cm of the anal canal [206, 210–212] and perhaps
attenuated anal squeeze pressures also [208, 210,
211], especially following treatment for transsphinc-
teric fistulas.

Haemorrhoidectomy
In terms of structures contributing to continence, the
sphincter muscles alone cannot entirely close the
anal lumen [213], and approximately 15% of the
basal anal canal resting tone is generated by the
expansile vascular anal cushions [214], which, along
with secondary anal mucosal folds [215], provide a
hermetic seal. The importance of these structures
becomes evident in patients with prolapsing haemor-
rhoids, where the mucocutaneous junction, which
provides a barrier against mucus and liquid faecal
leakage, may be displaced beyond the anal verge
[216]. Faecal soiling is not uncommon in such
patients [217] and may indeed be cured by haemor-
rhoidectomy [218, 219]. Contrarily, however, in con-
tinent patients with symptomatic haemorrhoids, sur-
gery is now clearly recognised as carrying a risk for
the development of incontinence.
There are essentially four varieties of haemor-
rhoidectomy: the open technique, now referred to as
the Milligan–Morgan operation [220]; the closed
technique, as popularised by Ferguson [221]; the
Parks submucosal technique [222]; and the more
recently introduced stapling method, as originally
described by Longo in 1998 [223]. Overall, several
large series (>380 patients) have shown that the inci-
dence of “severe” and persistent postoperative incon-
tinence is rare, ranging from 0.2–1%, irrespective of
surgical technique [224–227]. In addition, transient
soiling affecting 35–50% of patients may completely

resolve by 6 months [228, 229]. However, minor (fla-
tus) and moderate (soiling) incontinence has been
reported in the long term in a significant proportion
56
S.M. Scott, P.J. Lunniss
Chapter 4 Risk Factors in Faecal Incontinence
of patients. Johannsson et al. [230] showed that 33%
of patients suffered from disturbed continence up to 7
years following open haemorrhoidectomy; 29% of
these patients directly attributed onset of their incon-
tinence to the surgery. Guenin et al. [226] reported a
similar incidence of persistent soiling (27%) in 514
patients following closed haemorrhoidectomy. A ran-
domised trial comparing the Milligan–Morgan proce-
dure (109 patients) to the Ferguson technique (102
patients) favoured the latter with regard to develop-
ment of incontinence, with 13% in both groups suf-
fering from mild incontinence at 1 year. However,
only 1% had moderate incontinence following the
closed operation compared with 7% after the open
procedure [219].
Endoanal ultrasonography, performed in patients
complaining of incontinence following haemor-
rhoidectomy, has shown injury to the internal anal
sphincter in the majority. Abbasakoor et al. [231]
demonstrated an isolated internal anal sphincter
injury in 5/10 patients, a combined internal/external
anal sphincter in two and an isolated external anal
sphincter defect in one. Two patients had a normal
ultrasound [231]. Similarly, Lindsey et al. [181]

showed internal anal sphincter injury in 26 of 29
patients with incontinence following Milligan–Mor-
gan haemorrhoidectomy; the internal anal sphincter
was thin in 12 and disrupted in 14 at the pedicle exci-
sion sites. Furthermore, an adjacent external anal
sphincter injury was seen in 24% of patients. It has
also been suggested that loss of the endovascular
mucosal cushions contributes to the development of
incontinence [181, 231, 232].
Rectal Evacuatory Disorder
Faecal impaction is an important risk factor for
incontinence and predominantly affects older peo-
ple, especially those living in institutions [41, 95], but
also children [25, 41, 145]. In the elderly, approxi-
mately 50% of nursing home residents will suffer
from faecal incontinence [41, 233, 234]; prolonged
retention of stool in the rectum, perhaps secondary
to incomplete evacuation during defecation but also
as a consequence of other factors, such as physical
immobility, inadequate diet and water intake,
depression, dementia, associated metabolic disor-
ders (e.g. hypothyroidism) and use of constipating
drugs (e.g. narcotics, antipsychotics and antidepres-
sants), can lead to faecal impaction [95]. This may
result in overflow incontinence, which can be exacer-
bated by laxative use [235], which causes liquid stool
to seep around the faecal bolus [236]. The presence of
an impacted mass will also stimulate the secretion of
large volumes of mucus, which will further aggravate
the problem. Such overflow leakage has been attrib-

uted to a combination of decreased anorectal sensa-
tion and reduced anal pressures, possibly secondary
to persistent reflex inhibition of internal anal sphinc-
ter tone (although this concept has been challenged
[237]), which allows liquid stool to escape through
the anal canal [238]. Decreased rectal sensitivity and
increased rectal compliance may also contribute to
faecal retention by decreasing the frequency and
intensity of the desire (and hence the motivation) to
defecate [96].
Childhood constipation is a common problem,
affecting around 9% of children under 18 years [239].
In children without anorectal anomalies, functional
faecal retention, because of fear of painful defecation
or other reasons, may also result in faecal impaction
and encopresis or overflow soiling [25, 145]. Treat-
ment requires disimpaction, and education focused
on alleviating phobias and feelings of guilt by rein-
forcing self-esteem and incorporating disciplined
toileting behaviour [25]. Failure to “retrain” such
children may result in progressive dilatation of the
rectum (megarectum), leading to chronic impaction,
and in a proportion, symptoms may progress into
adulthood [240, 241].
Although a considerable body of literature is avail-
able regarding impaction-related incontinence at
both ends of the age spectrum (i.e. paediatrics/ado-
lescents and geriatrics), there is a relative paucity of
information in adults that addresses the concept that
rectal evacuatory dysfunction may be an independ-

ent risk factor for the involuntary loss of bowel con-
tents [59, 242–245] in spite of the fact that faecal
incontinence and “constipation” frequently coexist.
Passive (overflow) incontinence, or postdefecation
leakage, may occur as a consequence of incomplete
rectal emptying following defecation, secondary to a
“mechanical” (i.e. anatomical, such as large recto-
cele, intussusception, megarectum etc.) or “function-
al” (e.g. pelvic floor dyssynergia, poor defecatory
dynamics, nonrelaxing pelvic floor etc.) outlet
obstruction. As such, comprehension of the normal
process of defecation should be considered funda-
mental to the clinical management of patients with
incontinence, utilising techniques such as balloon
expulsion or barium or magnetic resonance (MR)
proctography.
Contemporary studies of the pathophysiology of
faecal seepage in adults also implicate impaired
(blunted) rectal sensation (i.e. hyposensitivity [246])
or increased compliance (i.e. a hypotonic rectum
[247, 248]), as seen in conditions of megarectum.
This results in the loss of a sense of urgency, faecal
impaction and overflow incontinence [249] in the
absence of an appropriate “compensatory” sphinc-
teric response [250–254]. In normal subjects, con-
57
scious contraction of the external anal sphincter
occurs in response to rectal distension, thus prevent-
ing incontinence of stool during reflex relaxation of
the internal anal sphincter (RAIR) [238]. This is cru-

cially dependent on perception of rectal distension
[255, 256]. However, the presence of diminished per-
ception of rectal distension will allow faecal material
to enter the rectum without conscious recognition,
and thus conscious contraction of the external anal
sphincter during reflex internal anal sphincter relax-
ation cannot occur [255, 257]. This results in a reduc-
tion in anal canal pressure and allows stool to enter
the anal canal, with the potential for passive leakage
[250, 258]. Rectal hyposensitivity may also underlie
dyssynergic defecation, exacerbating the retention of
faeces in the rectum [243, 254].
Furthermore, impaired perception of rectal dis-
tension may also leads to a shorter “warning”
between entry of stool into the rectum and impend-
ing defecation. This “late” recognition of a large fae-
cal bolus in the rectum, or the passage of stool into
the upper anal canal, may account for the sudden,
and apparently paradoxical, sense of extreme
urgency experienced by some patients with rectal
hyposensitivity [250, 259].
Rectal Prolapse
Faecal incontinence occurs in approximately two
thirds of patients with overt rectal prolapse [145,
260–263] and 30–40% of patients with symptomatic
rectal intussusception (covert or internal prolapse)
[264–266].
The pathophysiological basis for this incontinence
is unclear and likely to be multifactorial. Repeated
dilatation of the anal sphincter mechanism, which

may occur as a result of the descending prolapse,
may contribute to a dysfunctional internal anal
sphincter, resulting in reduced anal pressures [264,
267–269]. Commonly, the internal anal sphincter is
thickened, distorted or even fragmented on endoanal
ultrasound [270]. A reduction in thickness following
rectopexy suggests a partially reversible process
[271], and this is consistent with the finding that sur-
gical correction of prolapse/intussusception, which
decreases trauma to the internal anal sphincter,
improves continence, although often without a rise
in sphincter pressures [272–274]. Conversely, contin-
ued straining at stool over many years may lead to
perineal descent and has been proposed as a major
aetiological factor for the development of rectal
intussusception and prolapse [269, 275]. This may
further stretch and damage the pudendal nerves,
increasing the chances of faecal incontinence
[276–278]. Pudendal neuropathy has been found in
both continent and incontinent patients with bowel-
wall prolapse [269, 276, 279, 280], but it is less com-
mon and less severe in the continent group [279,
280]. However, the exact relationship between bowel-
wall descent, pudendal neuropathy and subsequent
faecal incontinence remains unclear. Prolapse may
also lead to chronic activation of the rectoanal
inhibitory function, with the descending bowel wall
acting as a space-occupying lesion in the rectal
lumen [268, 281, 282]. Other possible mechanisms
include reduced rectal capacity and compliance

[274], altered rectal sensorimotor function [269],
reversal of the anorectal pressure gradient [269] and
a decrease in rectosigmoid transit time [283], where-
by the presentation of a greater volume of stool to the
(possibly dysfunctional) rectum may stress the conti-
nence mechanism and contribute to incontinence.
References
1. MacArthur C, Bick DE, Keighley MR (1997) Faecal
incontinence after childbirth. Br J Obstet Gynaecol
104:46–50
2. Chaliha C, Kalia V, Stanton SL et al (1999) Antenatal
prediction of postpartum urinary and fecal inconti-
nence. Obstet Gynecol 94:689–694
3. MacLennan AH, Taylor AW, Wilson DH et al (2000)
The prevalence of pelvic floor disorders and their rela-
tionship to gender, age, parity and mode of delivery.
BJOG 107:1460–1470
4. MacArthur C, Glazener CM, Wilson PD, et al (2001)
Obstetric practice and faecal incontinence three
months after delivery. BJOG 108: 678–683
5. Eason E, Labrecque M, Marcoux S et al (2002) Anal
incontinence after childbirth. CMAJ 166: 326–330
6. Thorson AG (2002) Anorectal physiology. Surg Clin
North Am 82:1115–1123
7. Goldberg RP, Kwon C, Gandhi S et al (1992) Preva-
lence of anal incontinence among mothers of multi-
ples and analysis of risk factors. Am J Obstet Gynecol
189:1627–1630
8. Kok AL, Voorhorst FJ, Burger CW et al (1992) Urinary
and faecal incontinence in community–residing elder-

ly women. Age Ageing 21:211–215
9. Leigh RJ, Turnberg LA (1982) Faecal incontinence: the
unvoiced symptom. Lancet 1:1349–1351
10. Norderval S, Nsubuga D, Bjelke C et al (2004) Anal
incontinence after obstetric sphincter tears: incidence
in a Norwegian county. Acta Obstet Gynecol Scand
83:989–994
11. Davies MC, Creighton SM, Wilcox DT (2004) Long-
term outcomes of anorectal malformations. Pediatr
Surg Int 20:567–572
12. Levitt MA, Pena A (2005) Outcomes from the correc-
tion of anorectal malformations. Curr Opin Pediatr
17:394–401
13. Ong NT, Beasley SW (1991) Long-term continence in
patients with high and intermediate anorectal anom-
alies treated by sacroperineal (Stephens) rectoplasty. J
Pediatr Surg 26:44–48
58
S.M. Scott, P.J. Lunniss
Chapter 4 Risk Factors in Faecal Incontinence
14. Rintala R, Mildh L, Lindahl H (1994) Fecal continence
and quality of life for adult patients with an operated
high or intermediate anorectal malformation. J Pedi-
atr Surg 29:777–780
15. Rintala RJ, Lindahl H (1995) Is normal bowel function
possible after repair of intermediate and high anorec-
tal malformations? J Pediatr Surg 30:491–494
16. Verhoef M, Lurvink M, Barf HA et al (2005) High
prevalence of incontinence among young adults with
spina bifida: description, prediction and problem per-

ception. Spinal Cord 43:331–340
17. Lemelle JL, Guillemin F, Aubert D et al (2006) A mul-
ticentre study of the management of disorders of defe-
cation in patients with spina bifida. Neurogastroen-
terol Motil 18:123–128
18. Di Lorenzo C (1997) Chronic constipation and fecal
incontinence in children with neurological and neuro-
muscular handicap. J Pediatr Gastroenterol 25(Suppl
1):S37–S39
19. Morera C, Nurko S (2003) Rectal manometry in
patients with isolated sacral agenesis. J Pediatr Gas-
troenterol Nutr 37:47–52
20. Catto-Smith AG, Coffey CM, Nolan TM et al (1995)
Fecal incontinence after the surgical treatment of
Hirschsprung’s disease. J Pediatr 127:954–957
21. Fortuna RS, Weber TS, Trace JF Jr et al (1996) Critical
analysis of the operative treatment of Hirschsprung’s
disease. Arch Surg 131:520–524
22. Heikkenen M, Rintala RJ, Louhima I (1995) Bowel
function and quality of life in adult patients with oper-
ated Hirschsprung’s disease. Pediatr Surg Int
10:342–324
23. Loening-Baucke V (1998) Constipation in children. N
Engl J Med 339:1155–
1156
24. Baker SS, Liptak GS, Colletti RB et al (1999) Constipa-
tion in infants and children: evaluation and treatment.
A medical position statement of the North American
Society for Pediatric Gastroenterology and Nutrition. J
Pediatr Gastroenterol Nutr 29:612–626

25. Di Lorenzo C, Benninga MA (2004) Pathophysiology
of pediatric fecal incontinence. Gastroenterology
126(Suppl 1):S33–S40
26. Nakayama H, Jorgensen HS, Pedersen PM et al (1997)
Prevalence and risk factors of incontinence after
stroke. The Copenhagen Stroke study. Stroke 28:58–62
27. Harari D, Coshall C, Rudd AG et al (2003) New-onset
fecal incontinence after stroke: prevalence, natural
history, risk factors, and impact. Stroke 34:144–150
28. Ho YH, Goh HS (1995) Anorectal physiological
parameters in chronic constipation of unknown aeti-
ology (primary) and of cerebrovascular accidents–a
preliminary report. Ann Acad Med 24:367–368
29. Edwards LL, Pfiffer RF, Quigley EM et al (1991) Gas-
trointestinal symptoms in Parkinson’s disease. Mov
Disord 6:151–156
30. Mathers SE, Kempster PA, Law PJ et al (1989) Anal
sphincter dysfunction in Parkinson’s disease. Arch
Neurol 46:1061–1064
31. Edwards LL, Quigley EM, Harned RK et al (1994)
Characterization of swallowing and defecation in
Parkinson’s disease. Am J Gastroenterol 89:15–25
32. Ashraf W, Pfeiffer RF, Quigley EM (1994) Anorectal
manometry in the assessment of anorectal function in
Parkinson’s disease: a comparison with chronic idio-
pathic constipation. Mov Disord 9:655–663
33. Hinds JP, Eidelmann BH, Wald A (1990) Prevalence of
bowel dysfunction in multiple sclerosis. A population
study. Gastroenterology 98:1538
–1542

34. Chia YM, Fowler CJ, Kamm MA et al (1995) Prevalence
of bowel dysfunction in patients with multiple sclero-
sis and bladder dysfunction. J Neurol 242:105–110
35. Haldeman S, Glick M, Bhatia HH et al (1982) Colome-
try, cystometry, and evoked potentials in multiple
sclerosis. Arch Neurol 39:698–701
36. Krogh K, Christensen P, Laurberg S (2001) Colorectal
symptoms in patients with neurological disease. Acta
Neurol Scand 103:335–343
37. Sun WM, Read NW, Donnelly TC (1990) Anorectal
function in incontinent patients with cerebrospinal
disease. Gastroenterology 99:1372–1379
38. Talley NJ, Howell S, Jones MP et al (2002) Predictors of
turnover of lower gastrointestinal symptoms in dia-
betes mellitus. Am J Gastroenterol 97:3087–3094
39. Schiller LR, Santa Ana CA, Schmulen AC et al (1982)
Pathogenesis of fecal incontinence in diabetes melli-
tus: evidence of internal-anal-sphincter dysfunction.
N Engl J Med 307:1666–1671
40. Camilleri M, Bharucha AE (1996) Gastrointestinal
function in neurologic disease. Sem Neurol 16:203–216
41. Nelson RL (2004) Epidemiology of fecal incontinence.
Gastroenterology 126:S3–S7
42. Pretlove SJ, Radley S, Toozs-Hobson PM et al (2006)
Prevalence of anal incontinence according to age and
gender: a systematic review and meta-regression
analysis. Int Urogynecol J Pelvic Floor Dysfunct
17:407–417
43. Bannister JJ, Abouzekry L, Read NW (1987) Effect of
aging on anorectal function. Gut 28:353–357

44. Swash M, Gray A, Lubowski DZ et al (1988) Ultra-
structural changes in internal anal sphincter in neuro-
genic faecal incontinence. Gut 29:1692–1698
45. Jameson JS, Chia YW, Kamm MA et al (1994) Effect of
age, sex and parity on anorectal function. Br J Surg
81:1689–1692
46. Laurberg S, Swash M (1989) Effects of aging on the
anorectal sphincters and their innervation. Dis Colon
Rectum 32:737–742
47. Ryhammer AM, Laurberg S, Sorensen FH (1997)
Effects of age on anal function in normal women. Int J
Colorect Dis 12:225–229
48. Bharucha AE, Zinsmeister AR, Locke GR et al (2006)
Risk factors for fecal incontinence: a population-based
study in women. Am J Gastroenterol 101:1305–1312
49. Rao SS, Holdsworth CD, Read NW (1988) Symptoms
and stool patterns in patients with ulcerative colitis.
Gut 29:342–345
50. Farthing MJ, Lennard-Jones JE (1978) Sensibility of
the rectum to distension and the anorectal distension
reflex in ulcerative colitis. Gut 19:64–69
51. Rao SS, Read NW, Davison PA et al (1987) Anorectal
sensitivity and responses to rectal distention in
patients with ulcerative colitis. Gastroenterology
93:1270–1275
52. Buchmann P, Kolb E, Alexander-Williams J (1981)
Pathogenesis of urgency in defaecation in Crohn’s dis-
ease. Digestion 22:310–316
53. Bassotti G, de Roberto G, Chistolini F et al (2004)
Twenty-four-hour manometric study of colonic

59
propulsive activity in patients with diarrhea due to
inflammatory (ulcerative colitis) and non-inflamma-
tory (irritable bowel syndrome) conditions. Int J Col-
orect Dis 19:493–497
54. Loening-Baucke V, Metcalf AM, Shirazi S (1989) Rec-
tosigmoid motility in patients with quiescent and
active ulcerative colitis. Am J Gastroenterol 84:34–39
55. Longstreth GF, Thompson WG, Chey WD et al (2006)
Functional bowel disorders. Gastroenterology
130:1480–1491
56. Drossman DA, Sandler RS, Broom CM et al (1986)
Urgency and fecal soiling in people with bowel dys-
function. Dig Dis Sci 31:1221–1225
57. Talley NJ, Zinsmeister AR Van Dyke C et al (1991) Epi-
demiology of colonic symptoms and the irritable
bowel syndrome. Gastroenterology 101:927–934
58. Kwan AC, Hu WH, Chan YK et al (2002) Prevalence of
irritable bowel syndrome in Hong Kong. J Gastroen-
terol Hepatol 17:1180–1186
59. Kalantar JS, Howell S, Talley NJ (2002) Prevalence of
faecal incontinence and associated risk factors; an
underdiagnosed problem in the Australian communi-
ty? Med J Aust 176:54–57
60. Kellow JE, Azpiroz F, Delvaux M et al (2006) Applied
principles of neurogastroenterology: physiology/
motility sensation. Gastroenterology 130:1412–1420
61. Horowitz L, Farrar JT (1962) Intraluminal small intes-
tinal pressure in normal patients and in patients with
functional gastrointestinal disorders. Gastroenterolo-

gy 42:455–464
62. Kellow JE, Phillips SF (1987) Altered small bowel
motility in irritable bowel syndrome is correlated with
symptoms. Gastroenterology 92:1885–1893
63. Stivland T, Camilleri M, Vassallo M et al (1991) Scinti-
graphic measurement of regional gut transit in idio-
pathic constipation. Gastroenterology 101:107–115
64. Cann PA, Read NW, Brown C et al (1983) Irritable
bowel syndrome. Relationship of disorders in the tran-
sit of a single solid meal to symptom patterns. Gut
24:405–411
65. Vassallo M, Camilleri M, Phillips SF et al (1992) Tran-
sit through the proximal colon influences stool weight
in the irritable bowel syndrome. Gastroenterology
102:102–108
66. Ritchie J (1973) Pain from distension of the pelvic
colon by inflating a balloon in the irritable bowel syn-
drome. Gut 14:125–132
67. Whitehead WE, Engel BT, Schuster MM (1980) Irrita-
ble bowel syndrome: physiological and psychological
differences between diarrhea-predominant and con-
stipation-predominant patients. Dig Dis Sci
25:404–413
68. Chey WY, Jin HO, Lee MH et al (2001) Colonic motor
abnormality in patients with irritable bowel syndrome
exhibiting pain and diarrhea. Am J Gastroenterol
96:1499–1505
69. Quigley EMM (2006) Changing face of irritable bowel
syndrome. World J Gastroenterol 12:1–5
70. Hogston P (1987) Irritable bowel syndrome as a cause

of chronic pain in women attending a gynaecology
clinic. Br Med J 294:934–935
71. Prior A, Whorwell PJ (1989) Gynaecological consulta-
tion in patients with the irritable bowel syndrome. Gut
30:996–998
72. Parys BT, Haylen B, Hutton JL et al (1989) The effect of
simple hysterectomy on vesicourethral function. Br J
Urol 64:594–599
73. Taylor T, Smith AN, Fulton PM (1989) Effect of hys-
terectomy on bowel function. Br Med J 299:300–
301
74. Butler-Manuel SA, Buttery LD, A’Hern RP et al (2000)
Pelvic nerve plexus trauma at radical hysterectomy
and simple hysterectomy: the nerve content of the
uterine supporting ligaments. Cancer 89:834–841
75. Mundy AR (1982) An anatomical explanation for blad-
der dysfunction following rectal and uterine surgery.
Br J Urol 54:501–504
76. Symmonds RE, Williams TJ, Lee RA et al (1981)
Posthysterectomy enterocele and vaginal vault pro-
lapse. Am J Obstet Gynecol 140:852–859
77. Karasick S, Spettell CM (1997) The role of parity and
hysterectomy on the development of pelvic floor
abnormalities revealed by defecography. AJR Am J
Roentgenol 169:1555–1558
78. Smith AN, Varma JS, Binnie NR et al (1990) Disor-
dered colorectal motility in intractable constipation
following hysterectomy. Br J Surg 77:1361–1365
79. Varma JS (1992) Autonomic influences on colorectal
motility and pelvic surgery. World J Surg 16:811–819

80. Altman D, Zetterstrom J, Lopez A et al (2004) Effect of
hysterectomy on bowel function. Dis Colon Rectum
47:502–509
81. Farouk R, Duthie GS, Lee PW et al (1998) Endosono-
graphic evidence of injury to the internal anal sphinc-
ter after low anterior resection: long term follow-up.
Dis Colon Rectum 41:888–891
82. Parc R, Tiret E, Frileux P et al (1986) Resection and
colo-anal anastomosis with colonic reservoir for rectal
carcinoma. Br J Surg 73:139–141
83. Remzi FH, Fazio VW, Gorgun E et al (2005) Quality of
life, functional outcome, and complications of colo-
plasty pouch after anterior resection. Dis Colon Rec-
tum 48:735–743
84
. Machado M, Nygren J, Goldman S et al (2005) Func-
tional and physiologic assessment of the colonic reser-
voir or side-to-end anastomosis after low anterior
resection for rectal cancer: a two-year follow-up. Dis
Colon Rectum 48:29–36
85. Yo YH, Tan M, Leong AF et al (2000) Ambulatory
manometry in patients with colonic J-pouch and
straight coloanal anastomoses: randomized, con-
trolled trial. Dis Colon Rectum 43:793–799
86. Furst A, Burghofer K, Hutzel L et al (2002) Neorectal
reservoir is not the functional principle of the colonic
J-pouch: the volume of a short colonic J-pouch does
not differ from a straight coloanal anastomosis. Dis
Colon Rectum 45:660–667
87. Putta S, Andreyev HJ (2005) Faecal incontinence: a late

side-effect of pelvic radiotherapy. Clin Oncol
17:469–477
88. Varma JS, Smith AN, Busuttil A (1985) Correlation of
clinical and manometric abnormalities of rectal func-
tion following chronic radiation injury. Br J Surg
72:875–878
89. Pollack J, Holm T, Cedermark B et al (2006) Long-term
effect of preoperative radiation therapy on anorectal
function. Dis Colon Rectum 49:345–352
60
S.M. Scott, P.J. Lunniss
Chapter 4 Risk Factors in Faecal Incontinence
90. Lim JF, Tjandra JJ, Hiscocj R et al (2006) Preoperative
chemoradiation for rectal cancer caused prolonged
pudendal nerve terminal motor latency. Dis Colon
Rectum 49:12–19
91. Peeters KC, van de Velde CJ, Leer JW et al (2005) Late
side effects of short-course preoperative radiotherapy
combined with total mesorectal excision for rectal
cancer: increased bowel dysfunction in irradiated
patients–a Dutch colorectal cancer group study. J Clin
Oncol 23:6199–6206
92. Lunniss PJ, Gladman MA, Hetzer FH et al (2004) Risk
factors in acquired faecal incontinence. J R Soc Med
97:111–116
93. Kamm MA (1994) Obstetric damage and faecal incon-
tinence. Lancet 344:730–733
94. Rao SS (2004) Pathophysiology of adult fecal inconti-
nence. Gastroenterology 126(Suppl 1):S14–S22
95. Madoff RD, Parker SC, Varma MG, et al (2004) Faecal

incontinence in adults. Lancet 364:621–632
96. Bharucha AE (2003) Fecal incontinence. Gastroen-
terology 124:1672–1685
97. Sultan AH, Kamm MA, Hudson CN et al (1993) Anal-
sphincter disruption during vaginal delivery. N Engl J
Med 329:1905–1911
98. Donnelly V, Fynes M, Campbell D et al (1998) Obstet-
ric events leading to anal sphincter damage. Obstet
Gynecol 92:955–961
99. Zetterström JP, López A, Anzén B et al (1999) Anal
incontinence after vaginal delivery: a prospective
study in primiparous women. Br J Obstet Gynaecol
106:324–330
100. Donnelly V, O’Herlihy C, Campbell DM et al (1998)
Postpartum fecal incontinence is more common in
women with irritable bowel syndrome. Dis Colon Rec-
tum 41:586–589
101. Abramowitz L, Sobhani I, Ganansia R et al (2000) Are
sphincter defects the cause of anal incontinence after
vaginal delivery? Results of a prospective study. Dis
Colon Rectum 43:590–598
102. Pregazzi R, Sartore A, Bortoli P et al (2002) Immediate
postpartum perineal examination as a predictor of
puerperal pelvic floor dysfunction. Obstet Gynecol
99:581–584
103. Groutz A, Fait G, Lessing JB et al (1999) Incidence and
obstetric risk factors of postpartum anal incontinence.
Scand J Gastroenterol 34:315–318
104. Signorello LB, Harlow BL, Chekos AK et al (2000) Mid-
line episiotomy and anal incontinence: retrospective

cohort study. BMJ 320:86–90
105. Chaliha C, Sultan AH, Bland JM et al (2001) Anal func-
tion: effect of pregnancy and delivery. Am J Obstet
Gynecol 185:427–432
106. Hannah ME, Hannah WJ, Hodnett ED et al (2002) Out-
comes at 3 months after planned cesarean vs planned
vaginal delivery for breech presentation at term: the
international randomized Term Breech Trial. JAMA
287:1822–1831
107. Sartore A, De Seta F, Maso G et al (2004) The effects of
mediolateral episiotomy on pelvic floor function after
vaginal delivery. Obstet Gynecol 2004103:669–673
108. Chiarelli P, Murphy B, Cockburn J (2003) Fecal incon-
tinence after high-risk delivery. Obstet Gynecol
102:1299–1305
109. Wang A, Guess M, Connell K et al (2006) Fecal incon-
tinence: a review of prevalence and obstetric risk fac-
tors. Int Urogynecol J Pelvic Floor Dysfunct
17:253–260
110. Pollack J, Nordenstam J, Brismar S (
2004) Anal incon-
tinence after vaginal delivery: a five-year prospective
cohort study. Obstet Gynecol 104:1397–1402
111. Faltin DL, Otero M, Petignat P et al (2006). Women’s
health 18 years after rupture of the anal sphincter dur-
ing childbirth: I. Faecal incontinence. Am J Obstet
Gynecol 194:1255–1259
112. Fornell EU, Wingren G, Kjolhede P (2004) Factors
associated with pelvic floor dysfunction with emphasis
on urinary and fecal incontinence and genital pro-

lapse: an epidemiological study. Acta Obstet Gynecol
Scand 83:383–389
113. Ryhammer AM, Bek KM, Laurberg S (1995) Multiple
vaginal deliveries increase the risk of permanent
incontinence of flatus urine in normal premenopausal
women. Dis Colon Rectum 38:1206–1209
114. Guise JM, Morris C, Osterweil P et al (2007) Incidence
of fecal incontinence after childbirth. Obstet Gynecol
109:281–288
115. Poen AC, Felt-Bersma RJ, Dekker GA et al (1997)
Third degree obstetric perineal tears: risk factors and
the preventive role of mediolateral episiotomy. Br J
Obstet Gynaecol 104:563–566
116. Wood J, Amos L, Rieger N (1999) Third degree anal
sphincter tears: risk factors and outcome. Aust N Z J
Obstet Gynaecol 38:414–417
117. de Leeuw JW, Struijk PC, Vierhout ME et al (2001)
Risk factors for third degree perineal ruptures during
delivery. BJOG 108:383–387
118. Jander C, Lyrenas S (2001) Third and fourth degree
perineal tears. Predictor factors in a referral hospital.
Acta Obstet Gynecol Scand 80:229–234
119. Handa VL, Danielsen BH, Gilbert WM (2001) Obstet-
ric anal sphincter lacerations. Obstet Gynecol
98:225–230
120. Christianson LM, Bovbjerg VE, McDavitt EC (
2003)
Risk factors for perineal injury during delivery. Am J
Obstet Gynecol 189:255–260
121. Gupta N, Kiran TU, Mulik V et al (2003) The inci-

dence, risk factors and obstetric outcome in primi-
gravid women sustaining anal sphincter tears. Acta
Obstet Gynecol Scand 82:736–743
122. Williams A (2003) Third-degree perineal tears: risk
factors and outcome after primary repair. J Obstet
Gynaecol 23:611–614
123. Fynes M, Donnelly V, Behan M et al (1999) Effect of
second vaginal delivery on anorectal physiology and
faecal continence: a prospective study. Lancet
354:983–986
124. Faltin DL, Boulvain M, Irion O et al (2000) Diagnosis
of anal sphincter tears by postpartum endosonogra-
phy to predict fecal incontinence. Obstet Gynecol
95:643–647
125. Belmonte-Montes C, Hagerman G, Vega-Yepez PA et
al (2001) Anal sphincter injury after vaginal delivery in
primiparous females. Dis Colon Rectum 44:1244–1248
126. Nazir M, Carlsen E, Nesheim BI (2002) Do occult anal
sphincter injuries, vector volume manometry and
delivery variables have any predictive value for bowel
61
symptoms after first time vaginal delivery without
third and fourth degree rupture? A prospective study.
Acta Obstet Gynecol Scand 81:720–726
127. Pinta TM, Kylanpaa ML, Teramo KA et al (2004)
Sphincter rupture and anal incontinence after first
vaginal delivery. Acta Obstet Gynecol Scand
83:917–922
128. Damon H, Bretones S, Henry L et al (2005) Long-term
consequences of first vaginal delivery-induced anal

sphincter defect. Dis Colon Rectum 48:1772–1776
129. Sultan AH, Stanton SL (1997) Occult obstetric trauma
and anal incontinence. Eur J Gastroenterol Hepatol
9:423–427
130. Nygaard IE, Rao SS, Dawson JD (1997) Anal inconti-
nence after anal sphincter disruption: a 30-year retro-
spective cohort study. Obstet Gynecol 89:896–901
131. Fitzpatrick M, O'Herlihy C (2001) The effects of labour
and delivery on the pelvic floor. Best Pract Res Clin
Obstet Gynaecol 15:63–79
132. Oberwalder M, Dinnewitzer A, Baig MK et al (2004)
The association between late-onset fecal incontinence
and obstetric anal sphincter defects. Arch Surg
139:429–432
133. Byrd LM, Hobbiss J, Tasker M (2005) Is it possible to
predict or prevent third degree tears? Colorectal Dis
7:311–318
134. Combs CA, Robertson PA, Laros RK Jr (1990) Risk fac-
tors for third-degree and fourth-degree perineal lacer-
ations in forceps and vacuum deliveries. Am J Obstet
Gynecol 163:100–104
135. Richter HE, Brumfield CG, Cliver SP et al (2002) Risk
factors associated with anal sphincter tear: a compari-
son of primiparous patients, vaginal births after
cesarean deliveries, and patients with previous vaginal
delivery. Am J Obstet Gynecol 187:1194–1198
136. Simhan H, Krohn M, Heine RP (2004) Obstetric rectal
injury: risk factors and the role of physician experi-
ence. J Matern Fetal Neonatal Med 16:271–274
137. Shiono P, Klebanoff MA, Carey JC (1990) Midline epi-

siotomies: more harm than good? Obstet Gynecol
75:765–770
138. Fenner DE, Genberg B, Brahma P et al (2003) Fecal and
urinary incontinence after vaginal delivery with anal
sphincter disruption in an obstetrics unit in the Unit-
ed States. Am J Obstet Gynecol 189:1543–1549
139. Fitzgerald MP, Weber AM, Howden N et al (2007) Risk
factors for anal sphincter tear during vaginal delivery.
Obstet Gynecol 109:29–34
140. Andrews V, Sultan AH, Thakar R et al (2006) Risk fac-
tors for obstetric anal sphincter injury: a prospective
study. Birth 33:117–122
141. Guendelman S, Thornton D, Gould J et al (2006)
Obstetric complications during labor and delivery:
assessing ethnic differences in California. Womens
Health Issues 16:189–197
142. Helwig JT, Thorp JM Jr, Bowes WA Jr et al (1993) Does
midline episiotomy increase the risk of third- and
fourth-degree lacerations in operative vaginal deliver-
ies? Obstet Gynecol 82:276–279
143. Lal M, H Mann C, Callender R et al (2003) Does
Cesarean delivery prevent anal incontinence? Obstet
Gynecol 101:305–312
144. Nelson RL, Westercamp M, Furner SE (2006) A sys-
tematic review of the efficacy of Cesarean section in
the preservation of anal continence. Dis Colon Rectum
49:1587–1595
145. Kamm MA (1988) Faecal incontinence. BMJ 316:
528–532
146. Law PJ, Kamm MA, Bartram CI (1991) Anal

endosonography in the investigation of faecal inconti-
nence. Br J Surg 78:
312–314
147. Nielsen MB, Hauge C, Pedersen JF et al (1993)
Endosonographic evaluation of patients with anal
incontinence: findings and influence on surgical man-
agement. AJR Am J Roentgenol 160:771–775
148. Zetterstrom J, Mellgren A, Jensen LL et al (1999) Effect
of delivery on anal sphincter morphology and func-
tion. Dis Colon Rectum 42:1253–1260
149. Fornell EK, Berg G, Hallbook O et al (1996) Clinical
consequences of anal sphincter rupture during vaginal
delivery. J Am Coll Surg 183:553–558
150. Rieger N, Schloithe A, Saccone G et al (1997) The effect
of a normal vaginal delivery on anal function. Acta
Obstet Gynecol Scand 76:769–772
151. Rieger N, Schloithe A, Saccone G et al (1998) A
prospective study of anal sphincter injury due to
childbirth. Scand J Gastroenterol 33:950–955
152. Lee SJ, Park JW (2000) Follow-up evaluation of the
effect of vaginal delivery on the pelvic floor. Dis Colon
Rectum 43:1550–1555
153. Willis S, Faridi A, Schelzig S (2002) Childbirth and
incontinence: a prospective study on anal sphincter
morphology and function before and early after vagi-
nal delivery. Langenbecks Arch Surg 387:101–107
154. Hojberg KE, Hundborg HH, Ryhammer AM (2003)
The impact of delivery on anorectal function in
women with and women without anal incontinence–a
prospective study. Int Urogynecol J Pelvic Floor Dys-

funct 14:38–45
155. Fornell EU, Matthiesen L, Sjodahl R (2005) Obstetric
anal sphincter injury ten years after: subjective and
objective long term effects. BJOG 112:312–316
156. Fynes M, Donnelly VS, O'Connell PR et al (1998)
Cesarean delivery and anal sphincter injury. Obstet
Gynecol 92:496
–500
157. Snooks SJ, Setchell M, Swash M et al (1984) Injury to
innervation of pelvic floor sphincter musculature in
childbirth. Lancet 2:546–550
158. Snooks SJ, Swash M, Henry MM et al (1986) Risk fac-
tors in childbirth causing damage to the pelvic floor
innervation. Int J Colorectal Dis 1:20–24
159. Snooks SJ, Swash M, Mathers SE et al (1990) Effect of
vaginal delivery on the pelvic floor: a 5-year follow-up.
Br J Surg 77:1358–1360
160. Sultan AH, Kamm MA, Hudson CN (1994) Pudendal
nerve damage during labour: prospective study before
and after childbirth. Br J Obstet Gynaecol 101:22–28
161. Tetzschner T, Sorensen M, Rasmussen OO et al (1995)
Pudendal nerve damage increases the risk of fecal
incontinence in women with anal sphincter rupture
after childbirth. Acta Obstet Gynecol Scand
74:434–440
162. Tetzschner T, Sorensen M, Jonsson L et al (1997)
Delivery and pudendal nerve function. Acta Obstet
Gynecol Scand 76:324–331
163. Rieger N, Wattchow D (1999) The effect of vaginal
62

S.M. Scott, P.J. Lunniss
Chapter 4 Risk Factors in Faecal Incontinence
delivery on anal function. Aust N Z J Surg 69:172–177
164. Allen RE, Hosker GL, Smith AR et al (1990) Pelvic
floor damage and childbirth: a neurophysiological
study. Br J Obstet Gynaecol 97:770–779
165. Zetterstrom J, Lopez A, Holmstrom B et al (2003)
Obstetric sphincter tears and anal incontinence: an
observational follow-up study. Acta Obstet Gynecol
Scand 82:921–928
166. Kiff ES, Barnes PR, Swash M (1984) Evidence of
pudendal neuropathy in patients with perineal descent
and chronic straining at stool. Gut 25:1279–1282
167. Engel AF, Kamm MA (1994) The acute effect of strain-
ing on pelvic floor neurological function. Int J Col-
orectal Dis 9:8–12
168. Felt-Bersma RJ, van Baren R, Koorevaar M et al (1995)
Unsuspected sphincter defects shown by anal
endosonography after anorectal surgery. A prospec-
tive study. Dis Colon Rectum 38:249–253
169. Eisenhammer S (1951) The surgical correction of
chronic internal anal (sphincteric) contracture. S Afr
Med J 25:486–489
170. Notaras MJ (1969) Lateral subcutaneous sphincteroto-
my for anal fissure–a new technique. Proc R Soc Med
62:713
171. Khubchandani IT, Reed JF (1989) Sequelae of internal
sphincterotomy for chronic fissure in ano. Br J Surg
76:431–434
172. Pernikoff BJ, Eisenstat TE, Rubin RJ et al (1994) Reap-

praisal of partial lateral internal sphincterotomy. Dis
Colon Rectum 37:1291–1295
173. Richard CS, Gregoire R, Plewes EA et al (2000). Inter-
nal sphincterotomy is superior to topical nitroglycerin
in the treatment of chronic anal fissure: results of a
randomized, controlled trial by the Canadian Colorec-
tal Surgical Trials Group. Dis Colon Rectum
43:1048–
1057
174. Mentefl BB, Tezcaner T, Yilmaz U et al (2006) Results
of lateral internal sphincterotomy for chronic anal fis-
sure with particular reference to quality of life. Dis
Colon Rectum 49:1045–1051
175. Garcia-Aguilar J, Belmonte C, Wong WD et al (1996)
Open vs closed sphincterotomy for chronic anal fis-
sure: long-term results. Dis Colon Rectum 39:440–443
176. Nyam DC, Pemberton JH (1999) Long-term results of
lateral internal sphincterotomy for chronic anal fis-
sure with particular reference to incidence of fecal
incontinence. Dis Colon Rectum 42:1306–1310
177. Littlejohn DR, Newstead GL (1997) Tailored lateral
sphincterotomy for anal fissure. Dis Colon Rectum
40:1439–1442
178. Usatoff V, Polglase AL (1995) The longer term results
of internal anal sphincterotomy for anal fissure. Aust
N Z J Surg 65:576–578
179. Rotholtz NA, Bun M, Mauri MV et al (2005) Long-term
assessment of fecal incontinence after lateral internal
sphincterotomy. Tech Coloproctol 9:115–118
180. Casillas S, Hull TL, Zutshi M et al (2005) Incontinence

after a lateral internal sphincterotomy: are we under-
estimating it? Dis Colon Rectum 48:1193–1199
181. Lindsey I, Jones OM, Smilgin-Humphreys MM et al
(2004) Patterns of fecal incontinence after anal sur-
gery. Dis Colon Rectum 47:1643–1649
182. Sultan AH, Kamm MA, Nicholls RJ et aI (1994)
Prospective study of the extent of internal anal sphinc-
ter division during lateral sphincterotomy. Dis Colon
Rectum 37:1031–1033
183. Farouk R, Monson JR, Duthie GS (1997) Technical fail-
ure of lateral sphincterotomy for the treatment of
chronic anal fissure: a study using endoanal ultra-
sonography. Br J Surg 84:84–
85
184. Tjandra JJ, Han WR, Ooi BS et al (2001) Faecal incon-
tinence after lateral internal sphincterotomy is often
associated with coexisting occult sphincter defects: a
study using endoanal ultrasonography. ANZ J Surg
71:598–602
185. Zbar AP, Beer-Gabel M, Chiappa AC et al (2001) Fecal
incontinence after minor anorectal surgery. Dis Colon
Rectum 44:1610–1619
186. Lord PH (1968) A new regime for the treatment of
haemorrhoids. Proc R Soc Med 61:935–936
187. Steele SR, Madoff RD (2006) Systematic review: the
treatment of anal fissure. Aliment Pharmacol Ther
24:247–257
188. McCaffrey J (1975) Lord treatment of haemorrhoids.
Four-year follow-up of fifty patients. Lancet 1:133–134
189. MacDonald A, Smith A, McNeill AD et al (1992) Man-

ual dilatation of the anus. Br J Surg 79:1381–1382
190. Oliver DW, Booth MW, Kernick VF et al (1998) Patient
satisfaction and symptom relief after anal dilatation.
Int J Colorectal Dis 13:228–231
191. Konsten J, Baeten CG (2000) Hemorrhoidectomy vs.
Lord's method: 17-year follow-up of a prospective,
randomized trial. Dis Colon Rectum 43:503–536
192. Saad AM, Omer A (1992) Surgical treatment of chron-
ic fissure-in-ano: a prospective randomised study.
East Afr Med J 69:613–615
193. Nielsen MB, Rasmussen OO, Pedersen JF et al (1993)
Risk of sphincter damage and anal incontinence after
anal dilatation for fissure-in-ano. An endosonograph-
ic study. Dis Colon Rectum 36:677–
680
194. Lindsey I, Jones OM, Cunningham C et al (2004)
Chronic anal fissure. Br J Surg 91:270–279
195. Jensen SL, Lund F, Nielsen OV et al (1984) Lateral sub-
cutaneous sphincterotomy versus anal dilatation in
the treatment of fissure in ano in outpatients: a
prospective randomised study. Br Med J 289:528–530
196. Nelson R (2002) Operative procedures for fissure in
ano. Cochrane Database Syst Rev 2:CD002199
197. Snooks S, Henry MM, Swash M (1984) Faecal inconti-
nence after anal dilatation. Br J Surg 71:617–618
198. Speakman CT, Burnett SJ, Kamm MA et al (1991)
Sphincter injury after anal dilatation demonstrated by
anal endosonography. Br J Surg 78:1429–1430
199. Hammond TM, Knowles CH, Porrett T et al (2006) The
Snug Seton: short and medium term results of slow fis-

tulotomy for idiopathic anal fistulae. Colorectal Dis
8:328–337
200. Rosa G, Lolli P, Piccinelli D et al (2006) Fistula in ano:
anatomoclinical aspects, surgical therapy and results
in 844 patients. Tech Coloproctol 10:215–221
201. Sygut A, Zajdel R, Kedzia-Budziewska R et al (2007)
Late results of treatment of anal fistulas. Colorectal Dis
9:151–158
202. Sainio P, Husa A (1985) Fistula-in-ano. Clinical fea-
tures and long-term results of surgery in 199 adults.
Acta Chir Scand 151:169–176
63
203. van Tets WF, Kuijpers HC (1994) Continence disor-
ders after anal fistulotomy. Dis Colon Rectum
37:1194–1197
204. Garcia-Aguilar J, Belmonte C, Wong WD et al (1996)
Anal fistula surgery. Factors associated with recur-
rence and incontinence. Dis Colon Rectum 39:723–729
205. Williams JG, MacLeod CA, Rothenberger DA et al
(1991) Seton treatment of high anal fistulae. Br J Surg
78:1159–1161
206. Lunniss PJ, Kamm MA, Phillips RK (1994) Factors
affecting continence after surgery for anal fistula. Br J
Surg 81:1382–1385
207. Graf W, Pahlman L, Ejerblad S (1995) Functional
results after seton treatment of high transsphincteric
anal fistulas. Eur J Surg 161:289–291
208. Hamalainen KP, Sainio AP (1997) Cutting seton for
anal fistulas: high risk of minor control defects. Dis
Colon Rectum 40:1443–1446

209. Pescatori M, Ayabaca S, Caputo D (2004) Can anal
manometry predict anal incontinence after fistulecto-
my in males? Colorectal Dis 6:97–102
210. Belliveau P, Thomson JP, Parks AG. Fistula-in-ano (1983)
A manometric study. Dis Colon Rectum 26:152–154
211. Sainio P (1985) A manometric study of anorectal func-
tion after surgery for anal fistula, with special refer-
ence to incontinence. Acta Chir Scand 151:695–700
212. Chang SC, Lin JK (2003) Change in anal continence
after surgery for intersphincteral anal fistula: a func-
tional and manometric study. Int J Colorectal Dis
18:111–115
213. Gibbons CP, Trowbridge EA, Bannister JJ et al (1986
)
Role of anal cushions in maintaining continence.
Lancet 1:886–888
214. Lestar B, Penninckx F, Kerrimans R (1989) The com-
position of the anal basal pressure. An in vivo and in
vitro study in man. Int J Colorect Dis 4:118–122
215. Rao SS (2004) Diagnosis and management of fecal
incontinence. Am J Gastroenterol 99:1585–1604
216. Rasmussen OØ (1994) Anorectal function. Dis Colon
Rectum 37:386–403
217. Read MG, Read NW, Haynes WG et al (1982) A
prospective study of the effect of haemorrhoidectomy
on sphincter function and faecal continence. Br J Surg
69:396–398
218. Murie JA, Sim AJ, Mackenzie I (1982) Rubber band lig-
ation versus haemorrhoidectomy for prolapsing
haemorrhoids: a long term prospective clinical trial.

Br J Surg 69:536–538
219. Johannsson HO, Pahlman L, Graf W (2006) Random-
ized clinical trial of the effects on anal function of Mil-
ligan-Morgan versus Ferguson haemorrhoidectomy.
Br J Surg 93:1208–1214
220. Milligan ETC, Morgan CN, Jones LE et al (1937) Surgi-
cal anatomy of the anal canal and operative treatment
of hemorrhoids. Lancet 2:1119–1124
221. Ferguson JA, Heaton JR (1959) Closed hemorrhoidec-
tomy. Dis Colon Rectum 2:176–179
222. Parks AG (1956) The surgical treatment of haemor-
rhoids. Br J Surg 43:337–351
223. Longo A (1998) Treatment of haemorrhoids disease by
reduction of mucosa and haemorrhoidal prolapse with
circular suturing device: a new procedure. In: Pro-
ceedings of the 6th World Congress of Endoscopic
Surgery, Rome, pp 777–784
224. McConnell JC, Khubchandani IT (1983) Long-term
follow-up of closed hemorrhoidectomy. Dis Colon
Rectum 26:797–799
225. Ravo B, Amato A, Bianco V et al (2002) Complications
after stapled hemorrhoidectomy: can they be prevent-
ed? Tech Coloproctol 6:83–88
226. Guenin MO, Rosenthal R, Kern B et al (2005) Ferguson
hemorrhoidectomy: long-term results and patient sat-
isfaction after Ferguson's hemorrhoidectomy. Dis
Colon Rectum 48:1523–1527
227. Lan P, Wu X, Zhou X et al (2006) The safety and effi-
cacy of stapled hemorrhoidectomy in the treatment of
hemorrhoids: a systematic review and meta-analysis

of ten randomized control trials. Int J Colorectal Dis
21:172–178
228. Roe AM, Bartolo DC, Vellacott KD et al (1987) Sub-
mucosal versus ligation excision haemorrhoidectomy:
a comparison of anal sensation, anal sphincter
manometry and postoperative pain and function. Br J
Surg 74:948–951
229. Altomare DF, Rinaldi M, Sallustio PL et al (2001)
Long-term effects of stapled haemorrhoidectomy on
internal anal function and sensitivity. Br J Surg
88:1487–1491
230. Johannsson HO, Graf W, Pahlman L (2002) Long-term
results of haemorrhoidectomy. Eur J Surg 168:485–489
231. Abbasakoor F, Nelson M, Beynon J et al (1998) Anal
endosonography in patients with anorectal symptoms
after haemorrhoidectomy. Br J Surg 85:1522–1524
232. Jorge JM, Wexner SD (1993) Etiology and manage-
ment of fecal incontinence. Dis Colon Rectum
36:77–97
233. Tobin GW, Brocklehurst JC (1986) Faecal inconti-
nence in residential homes for the elderly: prevalence,
aetiology and management. Age Ageing 15:
41–46
234. Wald A (2005) Faecal incontinence in the elderly: epi-
demiology and management. Drugs Aging 22:131–139
235. Cooper ZR, Rose S (2000) Fecal incontinence: a clini-
cal approach. Mt Sinai J Med 67:96–105
236. Read NW, Abouzekry L, Read MG et al (1985) Anorec-
tal function in elderly patients with fecal impaction.
Gastroenterology 89:959–966

237. Read NW, Abouzekry L (1986) Why do patients with fae-
cal impaction have faecal incontinence. Gut 27:283–287
238. Loening-Baucke VA, Cruikshank BM (1986) Abnor-
mal defecation dynamics in chronically constipated
children with encopresis. J Pediatr 108:562–566
239. van den Berg MM, Benninga MA et al (2006) Epidemi-
ology of childhood constipation: a systematic review.
Am J Gastroenterol 101:2401–2409
240. van Ginkel R, Reitsma JB, Buller HA et al (2003) Child-
hood constipation: longitudinal follow-up beyond
puberty. Gastroenterology 125:357–363
241. Voskuijl WP, Reitsma JB, van Ginkel R et al (2006)
Longitudinal follow-up of children with functional
nonretentive fecal incontinence. Clin Gastroenterol
Hepatol 4:67–72
242. Rex DK, Lappas JC (1992) Combined anorectal
manometry and defecography in 50 consecutive adults
with fecal incontinence. Dis Colon Rectum
35:1040–1045
243. Rao SS, Ozturk R, Stessman M (2004) Investigation of
64
S.M. Scott, P.J. Lunniss
Chapter 4 Risk Factors in Faecal Incontinence
the pathophysiology of fecal seepage. Am J Gastroen-
terol 99:2204–2209
244. Scarlett Y (2004) Medical management of fecal incon-
tinence. Gastroenterology 126(Suppl 1):S55–S63
245. Shatari T, Hayes J, Pretlove S et al (2005) Importance
of evacuatory disturbance in evaluation of faecal
incontinence after third degree obstetric tear. Colorec-

tal Dis 7:18–21
246. Gladman MA, Lunniss PJ, Scott SM et al (2006) Rectal
hyposensitivity. Am J Gastroenterol 101:1140–1151
247. Siproudhis L, Bellissant E, Juguet F et al (1999) Per-
ception of and adaptation to rectal isobaric distension
in patients with faecal incontinence. Gut 44:687–692
248. Felt-Bersma RJ, Sloots CE, Poen AC et al (2000) Rectal
compliance as a routine measurement: extreme vol-
umes have direct clinical impact and normal volumes
exclude rectum as a problem. Dis Colon Rectum
43:1732–1738
249. Crowell MD (2004) Pathogenesis of slow transit and
pelvic floor dysfunction: from bench to bedside. Rev
Gastroenterol Disord 4(Suppl 2):S17–S27
250. Buser WD, Miner PB Jr (1986) Delayed rectal sensa-
tion with fecal incontinence. Successful treatment
using anorectal manometry. Gastroenterology
91:1186–1191
251. Lubowski DZ, Nicholls RJ (1988) Faecal incontinence
associated with reduced pelvic sensation. Br J Surg
75:1086–1088
252. Hoffmann BA, Timmcke AE, Gathright JB Jr et al
(1995) Fecal seepage and soiling: a problem of rectal
sensation. Dis Colon Rectum 38:746–748
253
. Gladman MA, Scott SM, Chan CL et al (2003) Rectal
hyposensitivity: prevalence and clinical impact in
patients with intractable constipation and fecal incon-
tinence. Dis Colon Rectum 46:238–246
254. Crowell MD, Lacy BE, Schettler VA et al (2004) Sub-

types of anal incontinence associated with bowel dys-
function: clinical, physiologic, and psychosocial char-
acterization. Dis Colon Rectum 47:1627–1635
255. Sun WM, Read NW, Miner PB (1990) Relation between
rectal sensation and anal function in normal subjects
and patients with faecal incontinence. Gut
31:1056–1061
256. Diamant NE, Kamm MA, Wald A et al (1999) AGA
technical review on anorectal testing techniques. Gas-
troenterology 116:735–760
257. Wald A, Tunuguntla AK (1984) Anorectal sensorimo-
tor dysfunction in fecal incontinence and diabetes
mellitus. Modification with biofeedback therapy. N
Engl J Med 310:1282–1287
258. Sun WM, Donnelly TC, Read NW (1992) Utility of a
combined test of anorectal manometry, electromyog-
raphy, and sensation in determining the mechanism of
‘idiopathic’ faecal incontinence. Gut 33:807–813
259. Smith AN, Binnie NR (1991) Neurological disorders.
In: Kumar D, Waldron DJ, Williams NS, eds. Clinical
measurement in coloproctology. Springer-Verlag,
London, pp 124–139
260. Broden G, Dolk A, Holmstrom B (1988) Recovery of
the internal anal sphincter following rectopexy: a pos-
sible explanation for continence improvement. Int J
Colorectal Dis 3:23–28
261. Williams JG, Wong WD, Jensen L et al (1991) Inconti-
nence and rectal prolapse: a prospective manometric
study. Dis Colon Rectum 34:209–216
262. Farouk R, Duthie GS (1998) Rectal prolapse and rectal

invagination. Eur J Surg 164:323–332
263. Kairaluoma MV, Kellokumpu IH (2005) Epidemiolog-
ic aspects of complete rectal prolapse. Scand J Surg
94:207–210
264. Ihre T, Seligson U (1975) Intussusception of the rec-
tum-internal procidentia: treatment and results in 90
patients. Dis Colon Rectum 18:391–396
265. Johansson C, Ihrs T, Ahlback SO (1985) Disturbances
in the defecation mechanism with special reference to
intussusception of the rectum (internal procidentia).
Dis Colon Rectum 27:435–441
266. Felt-Bersma RJ, Cuesta MA (2001) Rectal prolapse,
rectal intussusception, rectocele, and solitary rectal
ulcer syndrome. Gastroenterol Clin North Am
30:199–222
267. Frenckner B, Ihre T (1976) Function of the anal
sphincters in patients with intussusception of the rec-
tum. Gut 17:147–151
268. Mackle EJ, Parks TG (1986) The pathogenesis and
pathophysiology of rectal prolapse and solitary rectal
ulcer syndrome. Clin Gastroenterol 15:985–1002
269. Sun WM, Read NW, Donnelly TC et al (1989) A com-
mon pathophysiology for full thickness rectal pro-
lapse, anterior mucosal prolapse and solitary rectal
ulcer. Br J Surg 76:290–295
270. Dvorkin LS, Chan CL, Knowles CH et al (2004) Anal
sphincter morphology in patients with full-thickness
rectal prolapse. Dis Colon Rectum 47:198–203
271. Poen AC, de Brauw M, Felt-Bersma RJ et al (1996)
Laparoscopic rectopexy for complete rectal prolapse.

Clinical outcome and anorectal function tests. Surg
Endosc 10:904–908
272. Scaglia M, Fasth S, Hallgren T et al (1994) Abdominal
rectopexy for rectal prolapse. Influence of surgical
technique on functional outcome. Dis Colon Rectum
37:805–813
273. Schultz I, Mellgren A, Dolk A et al (1996) Continence
is improved after the Ripstein rectopexy. Different
mechanisms in rectal prolapse and rectal intussuscep-
tion? Dis Colon Rectum 39:300–306
274. Lazorthes F, Gamagami R, Cabarrot P et al (1998) Is
rectal intussusception a cause of idiopathic inconti-
nence? Dis Colon Rectum 41:602–605
275. Porter NH (1962) A physiological study of the pelvic
floor in rectal prolapse. Ann R Coll Surg Engl
31:379–404
276. Parks AG, Swash M, Urich H (1977) Sphincter dener-
vation in anorectal incontinence and rectal prolapse.
Gut 18:656–665
277. Jones PN, Lubowski DZ, Swash M et al (1987) Relation
between perineal descent and pudendal nerve damage
in idiopathic faecal incontinence. Int J Colorectal Dis
2:93–95
278. Lubowski DZ, Swash M, Nicholls RJ et al (1988)
Increase in pudendal nerve terminal motor latency
with defaecation straining. Br J Surg 75:1095–1097
279. Neill ME, Parks AG, Swash M (1981) Physiological
studies of the anal sphincter musculature in faecal
incontinence and rectal prolapse. Br J Surg 68:531–536
280. Roig JV, Buch E, Alos R et al (1998) Anorectal function

65
in patients with complete rectal prolapse. Differences
between continent and incontinent individuals. Rev
Esp Enferm Dig 90:794–805
281. Duthie GS, Bartolo DC (1992) Abdominal rectopexy
for rectal prolapse: a comparison of techniques. Br J
Surg 79:107–113
282. Farouk R, Duthie GS, MacGregor AB et al (1994) Rec-
toanal inhibition and incontinence in patients with
rectal prolapse. Br J Surg 81:743–746
283. Prokesch RW, Breitenseher MJ, Kettenbach J et al
(1999) Assessment of chronic constipation: colon tran-
sit time versus defecography. Eur J Radiol 32:197–203
66
S.M. Scott, P.J. Lunniss
Introduction: the Individual Behind the Diagnosis
There are many routes to becoming a patient with
faecal incontinence (FI), many aetiologies of the dis-
order, and many personal histories. The “meaning”
of the FI will be different for each patient, and his or
her way of managing it will depend not only on aeti-
ology but also on a number of personal, social and
medical factors. Is the FI secondary to a medical or
surgical mishap, or is it the by product of a life-sav-
ing surgical resection, an “act of God”, or an “act of
man”? Has the FI been with the patient since child-
hood, and has he or she developed coping strategies;
or is it of recent onset and as yet “new”, foreign and
unmanageable? What medical support is available to
the patient? What emotional support–from family,

partner, friends and work associates–is available? Is
the partner supportive, or resentful and disgusted?
What habitual defence mechanisms do, the patient
use in order to deal with adversity, and are these
mechanisms overall successful or counterproduc-
tive?
These are but a few questions we need to ask each
time a patient with FI presents in the clinic. In other
words, beyond the generalisations applying to
“patients” with FI lie individual men and women,
boys and girls, each with his or her own personal,
family, medical, psychological and social histories.
What applies to one patient or what works for a par-
ticular patient may not apply to or work for another.
Development of Bladder and Bowel Continence
Development of bladder and bowel continence is
intimately tied up with the development of the child
and his or her role as a competent human being.
Freud wrote about the power, pride and control of
the little prince on the potty: “His Majesty the Child”
[1]. The development of continence in a child is an
important developmental step and is praised and
rewarded throughout cultures. A crucial part of the
child’s development is the development of a sense of
self and the boundaries between “me” and “not me”.
Children learn that defecating in the wrong place
(pants), at the wrong time or in public is punished or
is the cause of humiliation or mockery, and that
there is pervasive disapproval of incontinence. Even
the word incontinence is linked with loss or lack of

control, with phrases in common parlance such as
“emotional incontinence” or “verbal incontinence”.
Very seldom, or perhaps never, is incontinence of
any sort seen as having any positive connotations.
As we grow older, the pleasurable sensations of defe-
cation are increasingly kept private [2–4]. Both in
the personal realm and in the social realm, defeca-
tion and faeces have become private and imbued
with shame and embarrassment [5–9]. Incontinence
is associated with negative images–of the mentally
unwell, the learning disabled, or demented elderly
patients.
We also know that secondary enuresis or encopre-
sis, i.e. the development of enuresis or encopresis
after the achievement of continence, is often associ-
ated with emotional or physical trauma in childhood.
So it should not surprise us that even when there is
an obvious physical aetiology for FI, this is some-
times exacerbated by psychological factors and can
be (at least partially) ameliorated by treatments that
address the patient’s psychology.
Stigma and Quality of Life
People with FI have been found to live in a restricted
world, often describing it as being similar to impris-
onment. The limits to their world are often dictated
by access to toilets, the need to carry a change of
clothing with them at all times, and attempts to con-
ceal the problem from family and friends alike.
There are few studies of people’s experiences of
living with FI, but one study of teenagers with FI

[10] found that the powerful social rules associated
with this area of life mean that families of teenagers
with FI faced public distaste, embarrassment,
ridicule, general ignorance and little opportunity for
Psychological Aspects of Faecal Incontinence
Julian M. Stern
5
discussion. A community-based research pro-
gramme [11] explored the feelings of exclusion sec-
ondary to FI. This study ran over the course of 5
years and involved a group of women suffering from
multiple sclerosis (MS). Some of the main concerns
in this group were in managing double inconti-
nence, the effects of MS on sexuality and sexual rela-
tionships, and trying to live well despite their chron-
ic illness. The shared group experience gave them
the freedom to talk openly about sex and inconti-
nence, subjects about which they had previously felt
compelled to be silent. Norton and Chelvanayagam
[12] ran two focus groups at St. Mark’s Hospital in
the UK to develop a research questionnaire titled
“Effects of Bowel Leakage”. For many participants,
this was the first time they had ever spoken openly
about their FI, and it was found to be mutually sup-
portive to be able to speak openly to peers about the
ever-present stress and risk of potential humilia-
tion. As with Australian women [11], access to toi-
lets and sexual relationships were cited as issues of
concern. However, what came through was evidence
of the extent to which all aspects of life were affect-

ed–skin care, shopping, food, employment, travel,
appearance and socialising, to name a few. Addi-
tional groups have been conducted at St. Mark’s for
patients with FI [13]. These groups have shown that
common themes include “symptom checking” with-
in the group; envying people with normal conti-
nence; sporadic anger towards the medical profes-
sion (as well as gratitude); problems with body
image, sexuality and sexual functioning; as well as
more complex intragroup dynamics, such as envy,
rivalry and resentment.
The relationship between FI and its impact on
quality of life (QOL) had been studied in the clinic
but not in the community until the study by
Bharucha et al. [14]. In that study, 23% of the subjects
with FI reported that the symptom had a moderate to
severe impact on one or more domains of QOL. This
figure is similar to the proportion of subjects (32%)
who reported that FI had “a lot of impact” on QOL in
a UK-based study [15]. The impact on QOL was
clearly related to severity of FI. Thus, 35% of patients
with moderate FI and 82% with severe FI reported a
moderate to severe impact on QOL [14].
The stigma involved accounts for the startling
finding that only 10% of women with FI had dis-
cussed the symptom with a physician in the past year.
Whitehead [16], in an editorial accompanying the
study by Bharucha et al. [14], described this finding
as “astonishing”, especially as the patients with
milder symptoms who are least likely to present to

their physicians are most likely to be helped by con-
servative measures. Whitehead wrote: “There is…
speculation that patients may be too embarrassed or
they may be too sceptical that anything can be done
about it” (p. 6). He suggested that researchers need to
investigate why patients with FI do not report this
symptom to their physicians and that there is a need
for the development of public education methods to
address this issue.
Sexuality
Little research has been performed on the effects of
bowel problems and FI on psychosexual functioning
in women. Trachter et al. [17] wrote whilst describing
irritable bowel syndrome (IBS): “While there is an
abundance of research addressing the medical
aspects of irritable bowel disease, the psychosexual
impact of these diseases is usually not targeted for
investigation” (p. 413). In recognition of this, Collings
and Norton [18] conducted a study to explore the
psychosocial and psychosexual aspects of women liv-
ing with FI. This was a small, exploratory study using
a semistructured interview format. The participants
reported a range of psychosexual issues, including
current lack of arousal or desire and abstinence.
Unexpectedly to the researchers, this was not a uni-
form problem, and seven of the 20 participants said it
was not really a problem unless FI occurred during
sexual contact.
Depression, Shame and Isolation
In the study by Collings and Norton [18], shame and

embarrassment were common, and depression,
stress, isolation, secrecy, poor self-image and sexual
avoidance or aversion were also reported. These nar-
rative-based findings tie in well with results from
other studies.
Amongst adolescents with FI, psychosocial
impairment was significant on the Child Assessment
Schedule, the Child Behaviour Checklist and the
Youth Self Report [19]. In a study of community-
dwelling adults, FI was found to have a marked neg-
ative effect on sexuality and job function and in some
cases led to near total social isolation as a result of
embarrassment.
Fisher et al. [20] used the Hospital Anxiety and
Depression Scale (HADS) on patients with FI. They
found that patients who had unsuccessful surgical
intervention had significantly higher scores than did
subjects with FI who had successful surgical out-
comes. This finding mirrors several investigations in
the urinary incontinence literature in which patients
showed elevated levels of distress when treatment for
incontinence was unsuccessful and no longer showed
such elevations when treatment was successful
68
J.M. Stern
Chapter 5 Psychological Aspects of Faecal Incontinence
[21–25]. Additional associations exist between FI and
anxiety, a fear of going out (which needs to be distin-
guished from the more traditional psychiatric syn-
dromes of agoraphobia/panic in the absence of FI),

poor sleep (especially in those patients who suffer
from nocturnal FI) and in some cases, the use of alco-
hol, and drugs such as hypnotics or illicit drugs.
Coping mechanisms identified by 20 patients with
FI in the study by Collings and Norton [18] included
practical and psychological measures, such as:
restricting activity (five), knowing the location of toi-
lets when out (five), care of diet or fasting (three), sep-
arate bedrooms (three), wearing pads (five), denial
(five), counselling (five) and turning to religion (one).
Psychological Assessment of the Patient with FI
Psychological assessment of the patient with FI
requires a confidential setting that gives the patient a
sense of being respected, carefully attended to and
not rushed. In our experience at St. Mark’s Hospital,
it is helpful if the patient recognises he or she is being
seen by a mental health professional associated with
a gastroenterology team who has an interest in and
empathy for such problems and is aware of the
shame, embarrassment and fear experienced by
many patients with FI. Patients are very sensitive to
the reactions of others to their FI and may (correctly
in some cases) fear that the mental health profes-
sional will be disgusted by the FI, just as other mem-
bers of the public may be (in fantasy or reality).
The initial moments in the assessment may
involve understanding something of the FI–its ori-
gins, its aetiology and the impact on the various
spheres of the patient’s life (family, friends, work
associates, occupation, sex, leisure, travel etc.). Usu-

ally, the patient is relieved to be able to talk about it
and sometimes will become tearful or very angry,
especially when there is a grievance (justified or
unjustified) against a surgeon, physician, nurse or
hospital. It is always important from the beginning to
look for features of depressed mood as well as resent-
ment, anger or the inability to express anger. In some
cases, there is a manic attitude, which incorporates
denial of the anguish involved, denial of the losses as
well as pain and stigma.
It is important to take a full personal and family
history, understanding something of the main rela-
tionships and attachment figures in the patient’s past
and present, as well as an educational and occupa-
tional history. It is crucial to understand aspects of
the patient’s social and psychosexual functioning,
both pre- and post-FI [25, 26]. A medical, psychiatric
and drug and/or alcohol history as well as some
understanding of the patient’s present circumstances
are also required. The patient’s own personality
structure and habitual way of coping and dealing
with difficulties and interpersonal relationships will
crucially colour his or her “relationship” to and
mode of coping with the FI.
In order to fully understand the impact of the FI
and its meaning to the individual patient, one must
also look for issues of shame, guilt and stigma. Is
there any sense that the patient feels he or she is to
blame for the FI? Does he or she “deserve it”? Is there
any secondary gain involved? Are there any symp-

toms or behaviours that might worsen the FI, such as
an unhelpful diet or any self-destructive behaviour?
(For a similar approach to patients, see Stern 2003a
and b [27, 28], and with particular reference to par-
enteral nutrition, see Stern 2006 [29]).
Other features of the assessment will include a brief
assessment of the patient’s cognitive functioning and
a mental-state examination to assess the presence of
a formal psychiatric condition. This assessment
requires expertise, patience, empathy and time.
Management
Following the assessment described above, manage-
ment strategies can be devised. This depends not only
on the patient’s psychological state but also on the
availability of treatments in each particular case. For
some patients, formal psychiatric management is
required, especially if there is severe depression (or
an anxiety disorder) that might benefit from pharma-
cotherapy. Whether or not pharmacotherapy is indi-
cated, it is almost invariably helpful for the patient if
there is also some psychological treatment available.
Psychological treatment can take many forms, rang-
ing from supportive counselling to cognitive behav-
ioural therapy (CBT) or in-depth psychoanalytic psy-
chotherapy [30, 31]. Treatment may be individual or
in a group setting, and we recently described both
group therapy and psychoeducational groups for
patients with FI [13]. As shown below, some of the
main themes from a brief psychotherapy group for
women with FI are similar to the main themes from a

psychoeducational group for women with FI:
Main themes from psychotherapy group meetings
for women with FI
– Symptom checking
– Disclosure of bowel and physical symptoms
– Experiences of health services
– Litigation
– Loss
– Sexual functioning
– Disability and hidden disability
– Employment
69
Main themes from psychoeducational group meet-
ings for women with FI
– Disclosure of bowel symptoms
– Seeking help and treatment
– Availability of and access to toilets
– Hidden disability
– Psychological aspects
Our experience in these group settings was that
not only do patients feel more empowered following
group treatment, they also on occasion report a less-
ening of the severity of their symptoms, indicating a
super-added psychogenic component to at least
some of the severity of the symptomatology.
Biofeedback has also been proven to have a beneficial
effect on patients with FI [32, 33] and is discussed else-
where in this volume. One should not underemphasise
the beneficial effects of the nurse–patient relationship in
the biofeedback therapy, one that provides the patient

not only with the specific techniques taught in the
biofeedback sessions, but crucially, a safe place in which
to talk to an empathetic confidante. The similarities
between this and the importance of the so-called “non-
specific factors” in psychotherapy are obvious [34].
Whilst the main focus so far in this chapter has
been on the patients’ psychological needs, we should
not forget the needs of two other groups–family mem-
bers, and professionals looking after these patients.
The impact on the family, spouse and children can be
immense, and support–be it through a social worker,
family therapist or groups for family members-should
be considered and made available where appropriate.
Professionals–for example, specialist nurses on the
wards or in the community–caring for these patients
have their own needs, too. The impact of dealing with
the incontinent patient cannot be underestimated,
and nurses (as with all of us!) have their own respons-
es to the reality of FI. None of us are immune from
emotions ranging from disgust to empathy, irritation
to overidentification, and sadness to reparative wish-
es. With this in mind, at St. Mark’s Hospital, we have
developed programmes to support specialist colo-
proctology nurses deal with the impact of their work
on their own psyches, addressing issues such as their
own feelings (countertransference) [29, 35, 36], as
well as providing all members of the multidisciplinary
team with a weekly forum in which to discuss prob-
lematic patients or patient–staff interactions. This
“care of the staff” is crucial in allowing staff members

to work productively and empathetically and to min-
imise the risk of staff “burnout”.
Conclusion
What I have proposed in this chapter is a psycholog-
ical approach to the patient with FI, recognising that,
for each patient, his or her FI will have a very indi-
vidual, unique meaning based on that person’s histo-
ry, relationships and psychological state. Assessment
of the patient’s psychological needs is a time-con-
suming but rewarding experience, and patients can
be helped by a variety of means to feel less alone, less
stigmatised and less disempowered. Medical staff
members, too, can benefit from a forum in which
these issues can be discussed. If these psychological
factors are denied, they may appear to have gone
away, but for the patient and for staff members, this
disappearance is illusory.
References
1. Freud S (1914) On narcissism: an introduction. In:
Strachey J (ed and trans) The standard edition of the
complete psychological works of Sigmund Freud, vol.
14. Hogarth Press, London, pp 73–102
2. Abraham K (1920) The narcissistic evaluation of
excretory processes in dreams and neuroses. In:
Selected papers of Karl Abraham. Hogarth Press, Lon-
don
3. Abraham K (1921) Contributions to the theory of the
anal character. In: Selected papers of Karl Abraham.
Hogarth Press, London
4. Freud S (1908) Character and anal erotism. In: Stra-

chey J (ed and trans). The standard edition of the com-
plete psychological works of Sigmund Freud. Hogarth
Press, London
5. Elias N (1978) The History of manners: The civilizing
process. New York: Pantheon books
6. Garcia JA, Crocker J, Wyman JF (2005) Breaking the
cycle of stigmatisation. J Wound Ostomy Continence
Nurs 32(1):38–52
7. Joachim G, Acorn S (2000) Stigma of visible and invis-
ible chronic conditions. J Adv Nurs 32(1):243–248
8. White C (1997) Living with a stoma. Sheldon Press,
London
9. Whorton JC (2000) Inner hygiene: constipation and
the pursuit of health in modern society. Oxford Uni-
versity Press, New York
10. Cavet J (1998) People don’t understand: children,
young people and their families living with a hidden
disability. National Children’s Bureau, London
11. Koch T, Selim P, Kralik D (2002) Enhancing lives
through the development of a community-based par-
ticipatory action research program. J Clin Nurs 11
(2):109–117
12. Norton C, Chelvanayagam S (2004) Bowel continence
nursing. Beaconsfield Publishers, Beaconsfield
13. Chelvanayagam S, Stern JM (2007) Using therapeutic
groups to support women with faecal incontinence? Br
J Nurs 16:214–218
14. Bharucha A, Zinsmeister A, Locke R et al (2005) Preva-
lence and burden of fecal incontinence: a population-
based study in women. Gastroenterology 129

:42–49
15. Perry S, Shaw C, McGrother C et al (2002) The preva-
lence of faecal incontinence in adults aged 40 years or
more living in the community. Gut 50:480–484
70
J.M. Stern
Chapter 5 Psychological Aspects of Faecal Incontinence
16. Whitehead W (2005) Diagnosing and managing faecal
incontinence: if you don’t ask, they won’t tell. Gas-
troenterology 129:6
17. Trachter AB, Rogers A, Leblum SR (2002) Inflamma-
tory bowel disease in women: impact on relationship
and sexual health. Inflamm Bowel Dis 8(6):413–421
18. Collings S, Norton C (2004) Women’s experiences of
faecal incontinence: a study. Br J Community Nurs
9(12):520–523
19. Diseth TH, Emblem R (1996) Somatic function, mental
health and psychological adjustment of adolescents
with anorectal anomalies. J Pediatr Surg 31:638–643
20. Fisher SE, Breckon K, Andrews H, Keighley M (1989)
Psychiatric screening for patients with faecal inconti-
nence or chronic constipation referred for surgical
treatment. Br J Surg 76:352–355
21. Hagglof B, Andren O, Bergstrom E et al (1998) Self-
esteem in children with nocturnal enuresis and uri-
nary incontinence. Eur Urol 33(Suppl 3):16–19
22. Burgio KL, Locher J, Roth D, Goode P (2001) Psycho-
logical improvements associated with behavioural and
drug treatment of urge incontinence in older women.
J Gerontol B Psychol Sci Soc 56:P46–P51

23. Millard RJ, Oldenburg B (1983) The symptomatic, uro-
dynamic and psychodynamic results of bladder re-
education programs. J Urol 130:715–719
24. Rosenzweig BA, Hischke D, Thomas S et al (1991)
Stress incontinence in women; psychological status
before and after treatment. J Reprod Med 36:835–838
25. Heymen S (2004) Psychological and cognitive vari-
ables affecting treatment outcomes for urinary and
fecal incontinence. Gastroenterology 126
:S146–151
26. Fenner DE, Genberg B, Brahama P et al (2003) Fecal
and urinary incontinence after vaginal delivery with
anal sphincter disruption in an obstetrics unit in the
United States. Am J Obstet Gynecol 189(6)1543–1550
27. Stern JM (2003a) Psychiatry, psychotherapy and gas-
troenterology: bringing it all together. Aliment Phar-
macol Ther 17:175–184
28. Stern JM (2003b) Stomas, sorrow and shame. In: Stig-
ma in healthcare: understanding the psychology of the
stigma of incontinence. Simon Foundation, Chicago
29. Stern JM (2006) Home parenteral nutrition and the
psyche: psychological challenges for patient and fami-
ly. Proceedings of the Nutrition Society, vol. 65(3).
CABI Publishing, Oxfordshire, pp 222–226
30. Montgomery C (2002) Role of dynamic group therapy
in psychiatry. Adv Psychiatr Treat 8(1):34–41
31. Vamos M (2006) Psychotherapy in the medically ill: a
commentary. Aus N Z J Psychiatry 40(4):295–309
32. Norton C, Kamm MA (1999) Outcome of biofeedback
for faecal incontinence. Br J Surg 86:1159–1163

33. Norton C, Chelvanayagam S, Wilson-Barnett, J et al
(2003) Randomised controlled trial of biofeedback for
fecal incontinence. Gastrtoenterology 125:1320–1329
34. Frank J (1961) Persuasion and healing. Johns Hopkins
Press, Baltimore
35. Stern JM (1999) Psychoanalytic psychotherapy in a
medical setting. Psychoanal Psychother 13(
1):51–68
36. Stern JM (2005) Psychotherapy-individual, family and
group. In: Wright P, Stern J, Phelan M. Core psychia-
try, 2nd edn. Elsevier Saunders, London, pp 541–564
71
Introduction
Given the psychological, social, and functional
impacts that fecal incontinence (FI) has on an indi-
vidual, the assessment of health-related quality of life
(HRQoL) is an important consideration when evalu-
ating the efficacy of treatment. An individual with FI
faces a serious set of challenges in living life, and as a
result, providers are also faced with consideration of
these issues in providing treatment. For example, the
implantation of an artificial sphincter is about more
than technical procedures; it is also about its impact
on the individual’s ability to live life.
The role of HRQoL continues to grow, and accom-
panying this growth is an increase in research in the
refinement of the assessment of HRQoL. HRQoL
assessment in FI is still relatively new, and the
process of specifying the range of issues involved as
well as the content of many of the areas identified to

date is ongoing. This work continues to improve the
understanding and knowledge of FI and expands
horizons. The following material focuses on two
issues associated with HRQoL assessment and FI.
First is a brief review of different measures that are
available to assess HRQoL for FI. This is followed by
a consideration of issues that are associated with
evaluating instruments for use in assessment of
HRQoL and the development of HRQoL instruments.
Existing Measures for Quality of Life in Fecal
Incontinence
The state of HRQoL measurement in FI is still devel-
oping and evolving. A number of reviews of issues
associated with and instruments available for meas-
uring HRQoL in FI are available [1–3]. What is
apparent from the research is that it is possible to
assess HRQoL in FI with success, but the field has by
no means matured.
There are three basic instrument types available
for the study of HRQoL in FI: (1) general HRQoL
instruments, (2) specialized instruments, and (3)
condition-specific measures. Each instrument sig-
nals a different approach and presents unique
strengths as well as associated weaknesses.
Instruments such as the SF-36 [4] and European
Quality of Life (EuroQol) [5] have been used with suc-
cess in numerous studies on FI. The primary concern
with the use of general HRQoL instruments is the sen-
sitivity of the instrument to specific issues associated
with FI as well as the presence of floor and ceiling

effects. While mixed, the findings are encouraging.
For example, the new version of the SF-36 (v 2.0)
appears to demonstrate increased sensitivity to
HRQoL in FI compared with the original SF-36 [6]. At
a minimum, these instruments can serve as gross
indicators of HRQoL in the FI population and provide
the opportunity to compare within as well as between
populations [e.g., urinary incontinence (UI) vs. FI].
This ability to compare across populations does
come with a price–a question about responsiveness
exists: Are the instruments sensitive enough to be
able to detect change that is meaningful in the FI
population? This issue is compounded with the
potential for floor effects emerging. When floor
effects are present, there is only one direction for
possible change to occur: towards improvement. As a
result, the measures can lead to a false conclusion-an
overestimation of benefit instead? Finally, when con-
sidering these measures, the specification of the
treatment outcome needs to be determined. Treat-
ment is often directed and specific, and thus gross
measures, such as general HRQoL instruments,
might not be able to detect meaningful changes rela-
tive to intended outcomes.
Specialized Measures
Specialized scales exist for an incredibly large range
of issues [7, 8], and research on QoL in FI could ben-
efit from their utilization in many instances. These
measures represent an underutilized area of HRQoL
assessment in FI. This underutilization detracts from

our ability to further the understanding of HRQoL in
Impact of Fecal Incontinence on Quality of Life
Todd H. Rockwood
6
FI. If a treatment, surgical or otherwise, is likely to be
strongly related to a specific aspect of HRQoL–e.g.,
stress/anxiety, depression, control–then selection of
specialized instruments that measure that domain
would best serve patients, providers, and researchers.
Condition-specific QoL (CSQoL) measures are
generally designed based on a model of disease/con-
dition causing change to some other construct, e.g.,
FI causes changes in the amount or intensity of anxi-
ety experienced by an individual. This assumption is
viable, and instruments such as the FIQoL scale make
the assumption that FI causes anxiety and the intent
is to assess anxiety solely associated with FI.
The above model is generally adequate for most
outcomes research, but it cannot be assumed to be
adequate for all research, nor is it adequate in the
long run. An example of this can actually be found in
the evaluation of instruments such as the FIQoL in
the postpartum population. This work consistently
points out that the assessment of core issues such as
shame, embarrassment, and stress are not complete-
ly adequate [9, 10]. This is due, in part, to the com-
bined presence of FI, the event of childbirth and a
newborn, and all the interactions that are not cap-
tured with general HRQoL or CSQoL instruments.
The use of specialized scales in these instances would

provide a more robust assessment and increase our
ability to evaluate the relativistic impacts of the dif-
ferent conditions.
Evaluation of specific treatments, such as biofeed-
back, could benefit greatly from the use of specialized
measures. Depression can be used as an example to
illustrate this benefit. Biofeedback targets control,
and depression is often a response to lack of control.
If biofeedback creates a sense of control, then as a sec-
ondary effect, biofeedback could impact depression.
Instruments designed specifically around depression,
such as the Beck Depression Inventory [7] or the Cen-
ter for Epidemiologic Studies Depression (CESD)
scale [7] would be more sensitive and likely to identi-
fy and assess such secondary impacts. Evaluation of
these secondary impacts would allow us to begin to
unravel an as of yet unanswered question: How much
does FI contribute to the emergence and manifesta-
tion of depression? Specialized scales would allow us
to begin to untangle these types of questions by start-
ing with depression and looking at how FI changes it
as opposed to the current approach in which we eval-
uate depression associated with FI. This knowledge
could then be used to refine CSQoL instruments.
Condition-specific Measures for Fecal Incontinence
Recent work on CSQoL measures in FI is encourag-
ing. This work is directed at three key issues: (1) eval-
uating the content of existing measures and pointing
out shortcomings, (2) comparing different measures
against each other to identify relative strengths and

weaknesses, and (3) developing new instruments or
refining the content of existing instruments in gener-
al or for application in specific populations.
Three instruments have dominated measurement
of HRQoL in FI. The Gastrointestinal Quality of Life
Index (GIQLI) [11], the Manchester Health Question-
naire [12], and the FIQL scale [13]. Each of these
instruments has been used successfully in the assess-
ment of QoL associated with treatment for with FI. A
number of other instruments have also been devel-
oped, but their utilization has not been as wide
spread. This is in part due to the very specific nature
of the instrument, e.g., QoL in a Parkinson’s disease
population [14], clinical/community epidemiology
[15, 16], or children [17].
An encouraging trend in QoL measurement in FI
is work that is building upon these base instruments.
For example, the sensitive and personal nature of FI
underscores the importance of how instruments are
administered. Kwon and colleagues have done work
to adapt the Manchester Health Questionnaire for
telephone administration [18]. Although the results
are not definitive, this does represent a critical step
[19].
Another encouraging area is work that points out
the shortcomings in these base tools, both conceptu-
ally and in terms of measurement. For example,
work has demonstrated the need to expand the con-
tent of the FIQoL to better capture the postpartum
mother’s experiences [9, 10]. Work such as this is

absolutely critical to improving our ability to meas-
ure QoL in FI.
Also underway is work that assesses QoL more
systemically. The GIQLI is the forerunner of work in
this area. It looks at FI within the context of the over-
all GI system. There are distinct benefits to such
instruments in that they focus on interrelated aspects
of the body so that, for example, function and effects
due to X [irritable bowel syndrome (IBS)] are not as
likely to be attributed to Y (FI). Recently, there has
been an increase of work focusing on measurement
associated with the pelvic floor and FI. Measures in
this area have a significant contribution to make. FI
is often associated with issues beyond the sphincter,
e.g., the pelvic floor, and as a result, its occurrence
cannot be disassociated from conditions such as UI.
Instruments such as the FIQoL might not be able to
disentangle QoL issues when both UI and FI are pres-
ent [9, 20, 21]. Instruments focusing on the pelvic
floor would be appropriate when the root cause of FI
is due to the pelvic floor but not appropriate for use
when FI is due to something other than the pelvic
floor (e.g., sphincter tear).
74
T.H. Rockwood
Chapter 6 Impact of Fecal Incontinence on Quality of Life
Health-related Quality of Life and Fecal
Incontinence
The following material focuses on central issues in
the consideration of what instrument(s) to use as

well as the development or refinement of existing
instruments. The primary question/issue is to deter-
mine what is meant by HRQoL relative to the pur-
pose of the research. Core to this is an assessment of
the primary and secondary impacts of treatment.
HRQoL can range from observable characteristics
(functional status) to abstract constructs that are not
directly observable (depression). Phenomena in the
latter instance are not straightforward when it comes
to conceptualization and measurement.
The notion of stress provides a good illustration of
the complexities associated with identifying or devel-
oping appropriate measures. Stress is a core issue
associated with HRQoL and FI, and the conceptual
orientation employed relative to stress can determine
both its meaning and how it is measured. Stress can
be conceptualized as event based or, alternatively, as
an internal coping phenomenon. In the event-based
model, stress is conceived of as an individual’s
response to events. An individual has an FI episode,
and this event causes stress. Stress is the result of the
event occurring; had the event not occurred, stress
would not be induced. Such a model is embedded
within much of the work in FI. The relativistic impact
of solid versus liquid stool loss events is an illustra-
tive example of such an approach. Alternatively, the
coping model does not focus on events that occur or
environmental conditions; rather, the focus is the
individual’s perception of their ability to deal with a
stress. In these instances, whether or not a stool loss

event has occurred is not particularly relevant. It is
the individual’s felt ability to cope with the event that
is important.
Consideration of scope is an oft-ignored issue in
the use HRQoL measures. Returning to the above
example of stress, consider two alternative studies: In
a surgical treatment of FI in which an artificial
sphincter is implanted, the focus on outcomes might
use a stress-events model. The intent of the artificial
sphincter is to reduce the number of events experi-
enced. Given this, in the assessment of HRQoL, logic
would argue that treatment reduces events and
reduction in events reduces stress. Alternatively, if
the research is focused on psychosocial interventions
(e.g., counseling to deal with postpartum FI), then a
different logic is employed; treatment increases abil-
ity to deal with FI occurring, and increased ability to
deal with FI reduces stress associated with FI. Recog-
nizing this distinction is important for both instru-
ment development as well as choosing between exist-
ing instruments when conducting studies. Concor-
dance between treatment outcomes and what is being
measured is essential to conducting good outcomes
research.
HRQoL can range from macro measures associat-
ed with existential well-being to micro measures
around shame and embarrassment associated with
FI. No single instrument can adequately represent
the full scope of HRQoL; instruments tend to focus
more or less on different aspects. This requires

thought when selecting an appropriate instrument.
FI is not a condition that has a primary effect on cog-
nitive abilities, but it does have a dramatic impact on
daily activities that are usually taken for granted
(e.g., shopping) or emotional and psychological con-
ditions (e.g., shame). The intent of CSQoL measures
such as the adapted Manchester Health Question-
naire [12, 18] or the FIQoL [13] is to focus on issues
that have high salience for FI. These instruments
tend to focus toward the microlevel measures in the
instrument and focus on the impact FI has on day-to-
day activities and life. The instruments do not
attempt to measure the impact that FI has on the
meaning of life.
Another critical issue in FI research is targeting
instruments for particular populations and/or situa-
tions. FI research is dominated by work in one of two
populations, geriatric or postpartum, with a smaller
amount of work in cancer, trauma, and adolescent
populations. HRQoL in general and CSQoL in partic-
ular is not uniform across populations, and consider-
ation of instrument needs to include an assessment
of the population. Instruments such as the GIQLI and
the FIQoL are designed for the general FI population,
and the unique situations faced by populations such
as the new mother or the institutionalized individual
bring fundamental changes to the conceptualization
of QoL. It is important that this aspect of scope be
included in the consideration of measures. Instru-
ments that adapt existing tools for use in specific

populations, such as the Manchester Health Ques-
tionnaire [12] or the work of Cockell et al. [10] for
postpartum or Trajanovska and Catto-Smith in chil-
dren [17], are central to expanding our knowledge
and understanding of FI.
One fundamental issue that has yet to be success-
fully dealt with in FI research is coping. To date, cop-
ing behaviors and mechanisms have been treated in
one of two ways in FI research. Figure 1a illustrates
the initial treatment of coping in FI research. Coping
is a response to severity and as a result is an indica-
tor of the severity of the condition. The impact of this
can mediate the impact severity has on HRQoL [22].
Alternatively, Figure 1 illustrates a more recent emer-
gence of the conceptualization of coping [3]. Coping
is related to severity as shown in the dashed line but
can be viewed as a response to severity or as a means
75
of reducing severity. Regardless, it has a direct rela-
tionship to HRQoL that has not yet been adequately
dealt with.
The final issue associated with conceptual issues
has been discussed within the context of the above,
but it is the purpose of the assessment of HRQoL. Is
the assessment aimed at evaluating the outcome of a
particular treatment, an epidemiological evaluation
of a population, or general social research evaluating
what FI means to life? To date, most instruments in
FI research have been developed around the assess-
ment of treatment and outcomes research. This

means that instrument content is dominated by
issues that should be either directly or indirectly
affected by treatment. Moving forward, instruments
need to evolve to reflect more of the individual’s
experience with FI as well as to make the instruments
more sensitive to evaluating treatment for FI.
Conclusions
FI is, as conditions go, an incredibly sensitive and
difficult issue to deal with relative to QoL assessment.
Whereas the condition is not necessarily life threat-
ening physically, it can be seen as life threatening for
social and personal life. Because of this, it is impor-
tant to assess QoL when treating or evaluating treat-
ment for FI.
Research has shown that the basic tools are avail-
able to assess HRQoL for individuals with FI and that
this assessment is a vital part of the evaluation of
treatment of FI. However, there is a need for addi-
tional work on QoL measurement in FI to refine the
understanding of basic issues, such as coping mech-
anisms, where they fit in relative to severity on the
QoL spectrum, and whether they provide sufficient
detail regarding shame and its role in QoL. Going for-
ward, there are several factors that can make work in
this area more successful and lead to more rapid
development: first is a focus on the development of
modules for specific populations that can be append-
ed to existing instruments. Second is building upon
the work that has been done to date and pushing it
forward, such as the work on QoL postpartum. Final-

ly is to start integrating the patient’s perspective into
measures at a deeper level.
References
1. Baxter NN, Rothenberger DA, Lowry AC (2003) Mea-
suring fecal incontinence. Dis Colon Rectum
46(12):1591–1605
2. Eton DT, Lepore SJ (2002) Prostate cancer and health-
related quality of life: a review of the literature. Psy-
chooncology 11(4):307–326
3. Rockwood TH (2004) Incontinence severity and QOL
scales for fecal incontinence. Gastroenterology 126
(1 Suppl 1):S106–S113
4. Ware J et al (1993) SF-36 Health Survey: manual and
interpretation guide. The Health Institute, New Eng-
land Medical Center, Boston
5. Brazier J, Jones N, Kind P (1993) Testing the validity of
the EuroQol and comparing it with the SF-36 Health
Survey questionnaire. Qual Life Res 2:169–180
6. Bordeianou L et al (2006) Does incontinence severity
correlate with quality of life? American Society of
Colon and Rectal Surgeons, Seattle, WA, June 2006
7. Robinson JP et al (1991) Measures of personality and
social psychological attitudes. In: Measures of social
psychological attitudes, vol 1. Academic Press, San
Diego
76
T.H. Rockwood
Fig. 1. Conceptualization of coping in fecal
incontinence research. HRQoL health-related
quality of life

Chapter 6 Impact of Fecal Incontinence on Quality of Life
8. McDowell I, Newell C (1996) Measuring health: a guide
to rating scales and questionnaires, 2nd edn. Oxford
University Press, New York
9. Hatem M, Fraser W, Lepire E (2005) Postpartum uri-
nary and anal incontinence: a population-based study
of quality of life of primiparous women in Quebec. J
Obstet Gynaecol Can 27(7):682–688
10. Cockell SJ, Oates-Johnson T, Gilmour DT et al (2003)
Postpartum flatal and Fecal Incontinence Quality-of-
Life Scale: a disease- and population-specific measure.
Qual Health Res 13(8):1132–1144
11. Eypasch E, Williams JI, Wood-Dauphinee S et al
(1995) Gastrointestinal Quality of Life Index: Develop-
ment, validation and application of a new instrument.
Br J Surg 82:216–222
12. Bug GJ, Kiff ES, Hosker G (2001) A new condition-spe-
cific health-related quality-of-life questionnaire for
the assessment of women with anal incontinence.
BJOG 108(10):1057–1067
13. Rockwood TH, Church JM, Fleshman JW et al (2000)
Fecal Incontinence Quality of Life Scale: quality-of-life
instrument for patients with fecal incontinence. Dis
Colon Rectum 43(1):9–16
14. Sakakibara R, Shinotoh H, Uchiyama T et al (2001)
Questionnaire-based assessment of pelvic organ dys-
function in Parkinson’s disease. Auton Neurosci
92(1–2):76–85
15. Bharucha AE, Locke GR 3rd, Seide BM, Zinsmeister
AR (2004) A new questionnaire for constipation and

faecal incontinence. Aliment Pharmacol Ther
20(3):355–364
16. Bharucha AE, Zinsmeister AR, Locke GR et al (2006)
Symptoms and quality of life in community women
with fecal incontinence. Clin Gastroenterol Hepatol
4(
8):1004–1009
17. Trajanovska M, Catto-Smith A-G (2005) Quality of life
measures for fecal incontinence and their use in chil-
dren. J Gastroenterol Hepatol 20(6):919–928
18. Kwon S, Visco AG, Fitzgerald MP et al (2005) Validity
and reliability of the Modified Manchester Health
Questionnaire in assessing patients with fecal inconti-
nence. Dis Colon Rectum 48(2):323–331
19. Rockwood T (2005) Comment: validity and reliability
of the Modified Manchester Health Questionnaire in
assessing patients with fecal incontinence. Dis Colon
Rectum 48(2):331–334
20. Barber MD, Walters MD, Bump RC (2005) Short forms
of two condition-specific quality-of-life question-
naires for women with pelvic floor disorders (PFDI-20
and PFIQ-7). Am J Obstet Gynecol 193(1):103–113
21. Kelly CE (2003) Which questionnaires should be used
in female urology practice? Curr Urol Rep
4(5):375–380
22. Jorge JM, Wexner SD (1993) Etiology and manage-
ment of fecal incontinence. Dis Colon Rectum
36(1):77–97
77
Introduction

Health care expenditure in the most economically
advanced countries seems to have spiraled out of
control over the last few decades. There are three
main reasons accounting for this situation: ageing of
the population has led to an increase in the numbers
requiring health care services, the accelerating pace
of technological development has given rise to new
techniques that have improved the quality of treat-
ment, and with the introduction of new, increasingly
costly, products, patient expectations have changed
and patients thus demand better medical treatment.
The combination of these three factors has resulted
in health care spending becoming increasingly diffi-
cult to control.
This means that the available resources must be
managed to the best advantage. Clearly, this implies
adopting the economic strategy that, according to
Samuelson’s [1] definition, consists of maximizing
the use of very limited resources that could be allo-
cated for other purposes.
The need to control health care expenditure initial-
ly prompted decision makers to consider implement-
ing investment cuts, with little regard for the long-
term repercussions that these could have. However, it
soon became apparent that to optimize the use of
resources allocated to health care, expenditure had to
be rationalized rather than rationed. Targeted objec-
tives of the health care policy (only the efficacy or only
the cost of a service) have, therefore, been superseded
by multidimensional objectives, which correlate the

efficacy of a program with the costs that it involves. In
this light, once clinical efficacy has been established,
health care programs must now be assessed in terms of
their economic efficiency (technical and allocational)
before a new therapeutic approach is introduced.
Economic Assessments in Health Care
An economic assessment is, by definition, “the com-
parative analysis of alternative courses of action in
terms of both their costs and consequences” [2]. The
steps to be taken in any assessment are, therefore, to
identify, measure, evaluate, and compare the costs
and consequences of the alternatives under consider-
ation. These operations apply to all fields, not the
least of which is health care services.
As various therapeutic options have to be consid-
ered, it is important that the alternatives to be com-
pared are homogeneous. The aim of rationalizing the
use of resources requires that costs and effects of a
program be compared with costs and effects of pro-
grams of the same kind, with a view to ascertaining
which is the most advantageous from an economic
standpoint. There are, in effect, no set rules govern-
ing the choice of the optimal alternative; however,
that optimal alternative should always be therapeuti-
cally significant (more frequently used and/or more
efficacious), readily available, and consistent with the
design of the study.
For the economic evaluation to be successful in
the field of health care, the purpose of the analysis
undertaken must be clarified, primarily to correctly

identify the costs and effects under consideration.
Cost is a subjective concept. Indeed, a cost must be
borne by someone, and assessment of the cost will,
therefore, depend on whom that someone is. In the
field of health care, an economic assessment can be
carried out from various points of view: the third-
party payer (insurer), the national health service
(NHS), the hospital facility, the patient, or society,
the latter comprising all the other categories. The
perspective of society is so vast that it embraces all
possible costs and effects. To adopt this perspective
would be simply too complicated, albeit more inter-
esting. Moreover, society as a whole is unlikely to
make direct decisions on the allocation of resources.
Having established the alternatives to be examined
and the perspective of the analysis, the problem
remains of quantifying costs (Table 1) and effects
(Table 2). Both can be subdivided into three catego-
ries: direct, indirect, and intangible. Direct costs can
be further subdivided into health care and non-health
care costs.
Social Aspects and Economics of
Fecal Incontinence
Carlo Ratto, Patrizia Ponzi, Francesca Di Stasi, Angelo Parello,
Lorenza Donisi, Giovanni B. Doglietto
7
Direct Costs
Health Care
Direct health care costs are those that can be directly
attributed to the procedures related to the diagnosis,

treatment, and rehabilitation involved in the man-
agement considered or necessary as a result of the
pathological conditions addressed by that manage-
ment.
Non-health Care
Non-health care costs comprise a range of expenses
directly related to the intervention considered but
which are not of a health care nature (e.g., the cost of
transporting patients).
Indirect Costs
Indirect costs are generally regarded as those due to
loss of productivity as a result of a pathological event
and the treatment thereof. Estimating these social
costs is one of the more difficult aspects encountered
in the economic appraisal of health care interven-
tions. Quantifying these costs is useful particularly
when the analysis technique is the most complete
and the perspective is the broadest, i.e., the perspec-
tive of society as a whole. Apart from the difficulty in
establishing true productivity losses, estimating
these costs often proves critical for various reasons.
Thus, with the exception of a few particular cases,
these costs are usually ignored.
Intangible Costs
Intangible costs are those borne by the individual as
a result of being in a poor state of health. These can-
not be assessed directly or evaluated in absolute
quantitative terms. Anxiety, stress, and pain are a few
examples. Quantifying these costs requires the use of
specific techniques and instruments ad hoc.

Direct Effects
These are the effects attributable to the diagnostic,
therapeutic, and rehabilitative procedures related to
the management of the case. These may manifest as
variations in objective clinical parameters, variations
in the probability of certain undesirable events such as
a heart attack or stroke, or variations in so-called final
consequences such as mortality or life expectancy.
Indirect Effects
These are generally interpreted as the effects arising
from the loss of productivity caused by the patholog-
ical condition and/or by the management adopted.
Intangible Effects
These refer to the effects on the individual due to the
impaired state of health. As these are of an intangible
nature, they cannot be assessed directly. They con-
cern psychological aspects such as anxiety, stress,
and pain that affect the patient’s quality of life. To
estimate these effects, specific techniques and ad hoc
instruments are required, as well as clinical indices
(erroneously defined as subjective) capable of esti-
mating the quality of life related to a specific type of
treatment or health condition.
Analysis Techniques
Essentially, four different techniques are used to per-
form the analyses, which, in order of increasing com-
80
C. Ratto, P. Ponzi, F. Di Stasi, A. Parello, L. Donisi, G.B. Doglietto
Table 1. Classification of costs and examples
Direct Indirect Intangible

Drugs
Hospitalization
Loss of work time Psychological factors
Diagnostics
Loss of earnings Impaired quality of
life
Rehabilitation
Home care
Table 2. Classification of effects and examples
Direct Indirect Intangible
Reduction in
costs of personnel
and materials
Reduction in
mortality
and morbidity Alleviation of pain
Reduction in costs
due to side-effects
Reduction in loss Improved quality
of productivity of life
Improvement in
clinical parameters